What is the function of the various brainwaves?It is well known that the brain is an electrochemical organ; researchers have speculated that a fully functioning brain can generate as much as 10 watts of electrical power. Other more conservative investigators calculate that if all 10 billion interconnected nerve cells discharged at one time that a single electrode placed on the human scalp would record something like five millionths to 50 millionths of a volt. If you had enough scalps hooked up you might be able to light a flashlight bulb.
Even though this electrical power is very limited, it does occur in very specific ways that are characteristic of the human brain. Electrical activity emanating from the brain is displayed in the form of brainwaves. There are four categories of these brainwaves, ranging from the most activity to the least activity. When the brain is aroused and actively engaged in mental activities, it generates beta waves. These beta waves are of relatively low amplitude, and are the fastest of the four different brainwaves. The frequency of beta waves ranges from 15 to 40 cycles a second. Beta waves are characteristics of a strongly engaged mind. A person in active conversation would be in beta. A debater would be in high beta. A person making a speech, or a teacher, or a talk show host would all be in beta when they are engaged in their work.
The Brainwaves
The next brainwave category in order of frequency is alpha. Where beta represented arousal, alpha represents non-arousal. Alpha brainwaves are slower, and higher in amplitude. Their frequency ranges from 9 to 14 cycles per second. A person who has completed a task and sits down to rest is often in an alpha state. A person who takes time out to reflect or meditate is usually in an alpha state. A person who takes a break from a conference and walks in the garden is often in an alpha state.
The next state, theta brainwaves, are typically of even greater amplitude and slower frequency. This frequency range is normally between 5 and 8 cycles a second. A person who has taken time off from a task and begins to daydream is often in a theta brainwave state. A person who is driving on a freeway, and discovers that they can't recall the last five miles, is often in a theta state--induced by the process of freeway driving. The repetitious nature of that form of driving compared to a country road would differentiate a theta state and a beta state in order to perform the driving task safely.
Individuals who do a lot of freeway driving often get good ideas during those periods when they are in theta. Individuals who run outdoors often are in the state of mental relaxation that is slower than alpha and when in theta, they are prone to a flow of ideas. This can also occur in the shower or tub or even while shaving or brushing your hair. It is a state where tasks become so automatic that you can mentally disengage from them. The ideation that can take place during the theta state is often free flow and occurs without censorship or guilt. It is typically a very positive mental state.
The final brainwave state is delta. Here the brainwaves are of the greatest amplitude and slowest frequency. They typically center around a range of 1.5 to 4 cycles per second. They never go down to zero because that would mean that you were brain dead. But, deep dreamless sleep would take you down to the lowest frequency. Typically, 2 to 3 cycles a second.
When we go to bed and read for a few minutes before attempting sleep, we are likely to be in low beta. When we put the book down, turn off the lights and close our eyes, our brainwaves will descend from beta, to alpha, to theta and finally, when we fall asleep, to delta.
It is a well known fact that humans dream in 90 minute cycles. When the delta brainwave frequencies increase into the frequency of theta brainwaves, active dreaming takes place and often becomes more experiential to the person. Typically, when this occurs there is rapid eye movement, which is characteristic of active dreaming. This is called REM, and is a well known phenomenon.
When an individual awakes from a deep sleep in preparation for getting up, their brainwave frequencies will increase through the different specific stages of brainwave activity. That is, they will increase from delta to theta and then to alpha and finally, when the alarm goes off, into beta. If that individual hits the snooze alarm button they will drop in frequency to a non-aroused state, or even into theta, or sometimes fall back to sleep in delta. During this awakening cycle it is possible for individuals to stay in the theta state for an extended period of say, five to 15 minutes--which would allow them to have a free flow of ideas about yesterday's events or to contemplate the activities of the forthcoming day. This time can be an extremely productive and can be a period of very meaningful and creative mental activity.
In summary, there are four brainwave states that range from the high amplitude, low frequency delta to the low amplitude, high frequency beta. These brainwave states range from deep dreamless sleep to high arousal. The same four brainwave states are common to the human species. Men, women and children of all ages experience the same characteristic brainwaves. They are consistent across cultures and country boundaries.
Research has shown that although one brainwave state may predominate at any given time, depending on the activity level of the individual, the remaining three brain states are present in the mix of brainwaves at all times. In other words, while somebody is an aroused state and exhibiting a beta brainwave pattern, there also exists in that person's brain a component of alpha, theta and delta, even though these may be present only at the trace level.
It has been my personal experience that knowledge of brainwave states enhances a person's ability to make use of the specialized characteristics of those states: these include being mentally productive across a wide range of activities, such as being intensely focused, relaxed, creative and in restful sleep.
Sunday, October 26, 2008
somatic mtDNA mutations with adult onset leukaemia
Mitochondria, the power house of the cell are under the control of genomic DNA (mtDNA) and nuclear DNA.The mtDNA is a 16.6 kb molecule, encodes 13 subunits of respiratory chain complexes, as well as 22 tRNA and two ribosomal RNA for intramitochondrial synthesis. Mutations in mitochondrial DNA (mtDNA) are frequent in cancers but it is not yet clearly established whether they are modifier events involved in cancer progression or whether they are a consequence of tumorigenesis. We therefore decided to determine the spectrum of somatic mtDNA mutation in adult-onset leukaemia by comparing directly the entire mitochondrial genome sequence from normal and leukemic cells obtained from 24 patients with both chronic and acute presentations. This comparison gives the change in nucleotide composition. On this basis we can repair those sequences and modify it by gene therapy. By doing this the problems of graft rejection and bone marrow replacement are solved and the disease leukaemia can be treated in a more efficient way.
Introduction: Mitochondria are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. In humans, mitochondrial DNA spans about 16,500 DNA building blocks (base pairs), representing a fraction of the total DNA in cells.
Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Mitochondrial DNA is prone to noninherited (somatic) mutations. Somatic mutations occur in the DNA of certain cells during a person’s lifetime and typically are not passed to future generations. Somatic mutations in mitochondrial DNA have been reported in some forms of cancer, including breast, colon, stomach, liver, and kidney tumours. These mutations also have been associated with cancer of blood-forming tissue (leukaemia) and cancer of immune system cells (lymphoma).
Somatic mutations in mitochondrial DNA may increase the production of potentially harmful molecules called reactive oxygen species. Mitochondrial DNA is particularly vulnerable to the effects of these molecules and has a limited ability to repair itself. As a result, reactive oxygen species easily damage mitochondrial DNA, causing a buildup of additional somatic mutations. Researchers continue to investigate how these mutations may lead to uncontrolled cell division and the growth of cancerous tumours.
The mtDNA is inherited from mother’s body. In case of sperm the maximum mtDNA stays in the tail which is isolated during fertilization. As a result the zygote gets only maternal mtDNA and no paternal DNA.
Materials and methods
Patients
24 adult patients (aged 18–88 years), six with acute lymphatic leukaemia (ALL), six with acute myeloid leukaemia (AML), six with chronic lymphatic leukaemia (CLL) and six with chronic myeloid leukaemia (CML) had been studied. All had been given their informed consent for these investigations, which were approved by the local Ethics Committee. Tumour samples were represented by bone marrow (ALL and AML), blood with high white blood cell count (CLL) or blood during therapy failure (CML). For each patient, buccal epithelial cells were collected from mouthwashes by centrifugation as representative of normal tissue.
mtDNA sequencing
DNA was extracted by standard procedures and the entire mitochondrial genome was amplified in 28 overlapping fragments of between 600 and 700 bp using M13-tagged oligodeoxynucleotide primers to facilitate the direct sequencing of the PCR-amplified products. A complete list of the primer pairs and sequencing protocol has been published previously.26 Briefly, following PCR amplification, samples were purified to remove unincorporated primers and sequenced directly using BigDye terminator cycle sequencing chemistries (PE Biosystems) on an ABI 377 automated DNA sequencer. The sequences obtained were compared directly to the revised Cambridge reference sequence (rCRS)27 using Sequence Navigator and Factura software (PE Biosystems) to identify sequence variants. Somatic mutations were identified by directly comparing the sequence differences detected in buccal and tumour samples from individual patients.
Introduction: Mitochondria are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. In humans, mitochondrial DNA spans about 16,500 DNA building blocks (base pairs), representing a fraction of the total DNA in cells.
Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Mitochondrial DNA is prone to noninherited (somatic) mutations. Somatic mutations occur in the DNA of certain cells during a person’s lifetime and typically are not passed to future generations. Somatic mutations in mitochondrial DNA have been reported in some forms of cancer, including breast, colon, stomach, liver, and kidney tumours. These mutations also have been associated with cancer of blood-forming tissue (leukaemia) and cancer of immune system cells (lymphoma).
Somatic mutations in mitochondrial DNA may increase the production of potentially harmful molecules called reactive oxygen species. Mitochondrial DNA is particularly vulnerable to the effects of these molecules and has a limited ability to repair itself. As a result, reactive oxygen species easily damage mitochondrial DNA, causing a buildup of additional somatic mutations. Researchers continue to investigate how these mutations may lead to uncontrolled cell division and the growth of cancerous tumours.
The mtDNA is inherited from mother’s body. In case of sperm the maximum mtDNA stays in the tail which is isolated during fertilization. As a result the zygote gets only maternal mtDNA and no paternal DNA.
Materials and methods
Patients
24 adult patients (aged 18–88 years), six with acute lymphatic leukaemia (ALL), six with acute myeloid leukaemia (AML), six with chronic lymphatic leukaemia (CLL) and six with chronic myeloid leukaemia (CML) had been studied. All had been given their informed consent for these investigations, which were approved by the local Ethics Committee. Tumour samples were represented by bone marrow (ALL and AML), blood with high white blood cell count (CLL) or blood during therapy failure (CML). For each patient, buccal epithelial cells were collected from mouthwashes by centrifugation as representative of normal tissue.
mtDNA sequencing
DNA was extracted by standard procedures and the entire mitochondrial genome was amplified in 28 overlapping fragments of between 600 and 700 bp using M13-tagged oligodeoxynucleotide primers to facilitate the direct sequencing of the PCR-amplified products. A complete list of the primer pairs and sequencing protocol has been published previously.26 Briefly, following PCR amplification, samples were purified to remove unincorporated primers and sequenced directly using BigDye terminator cycle sequencing chemistries (PE Biosystems) on an ABI 377 automated DNA sequencer. The sequences obtained were compared directly to the revised Cambridge reference sequence (rCRS)27 using Sequence Navigator and Factura software (PE Biosystems) to identify sequence variants. Somatic mutations were identified by directly comparing the sequence differences detected in buccal and tumour samples from individual patients.
immunosuppressant drugs
PURPOSE. To determine alterations in expression of genes in herpes simples virus (HSV)-1 latently infected mouse trigeminal ganglia (TGs), after treatment with cyclophosphamide and dexamethasone.
METHODS. Scarified corneas of female BALB/c mice were inoculated with HSV-1 strain McKrae. Four weeks after inoculation, cyclophosphamide and dexamethasone were intravenously injected to induce HSV-1 reactivation. Uninfected mice were also treated with the immunosuppressants. Four groups of animals were studied: uninfected, not treated; uninfected, drug treated; latently infected, not treated; and latently infected, drug treated. PolyA+ mRNA from the TGs of each group was reverse transcribed, labeled with 32P, incubated on a 1185-gene array membrane, and analyzed by phosphorimaging. As a comparison and to confirm microarray results, semiquantitative RT-PCR was also performed for selected genes.
RESULTS. The immunosuppressive drugs significantly increased expression of two genes (calpactin 1 light chain and guanine nucleotide-binding protein –stimulating polypeptide [GNAS]) in the ganglia of uninfected mice compared with those in untreated uninfected mice. Ten genes were shown to be significantly increased in the latent TGs of mice treated with immunosuppressants compared with latently infected untreated mice. These genes were prostaglandin E2 receptor EP4 subtype (PTGER4), insulin promoter factor 1 (IPF1), glutathione S-transferase µ2, cyclin D2, peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 proto-oncogene, and GNAS. Eight genes were shown to be significantly decreased in the HSV-1 latent TGs treated with the drugs, compared with untreated latently infected mice. These genes were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protein zero, mitogen-activated protein kinase 3, prothymosin beta 4, and brain lipid-binding protein. The results obtained by semiquantitative RT-PCR were similar to those obtained by microarray analysis.
CONCLUSIONS. Those genes with expression altered by immunosuppressive drug treatment may play an important role in ocular HSV-1 recurrence. Changes in expression of genes in the prostaglandin pathway, a transcription factor, and an enzyme in the cell cycle are considered especially important in HSV-1 reactivation by immunosuppression and are reviewed.
METHODS. Scarified corneas of female BALB/c mice were inoculated with HSV-1 strain McKrae. Four weeks after inoculation, cyclophosphamide and dexamethasone were intravenously injected to induce HSV-1 reactivation. Uninfected mice were also treated with the immunosuppressants. Four groups of animals were studied: uninfected, not treated; uninfected, drug treated; latently infected, not treated; and latently infected, drug treated. PolyA+ mRNA from the TGs of each group was reverse transcribed, labeled with 32P, incubated on a 1185-gene array membrane, and analyzed by phosphorimaging. As a comparison and to confirm microarray results, semiquantitative RT-PCR was also performed for selected genes.
RESULTS. The immunosuppressive drugs significantly increased expression of two genes (calpactin 1 light chain and guanine nucleotide-binding protein –stimulating polypeptide [GNAS]) in the ganglia of uninfected mice compared with those in untreated uninfected mice. Ten genes were shown to be significantly increased in the latent TGs of mice treated with immunosuppressants compared with latently infected untreated mice. These genes were prostaglandin E2 receptor EP4 subtype (PTGER4), insulin promoter factor 1 (IPF1), glutathione S-transferase µ2, cyclin D2, peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 proto-oncogene, and GNAS. Eight genes were shown to be significantly decreased in the HSV-1 latent TGs treated with the drugs, compared with untreated latently infected mice. These genes were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protein zero, mitogen-activated protein kinase 3, prothymosin beta 4, and brain lipid-binding protein. The results obtained by semiquantitative RT-PCR were similar to those obtained by microarray analysis.
CONCLUSIONS. Those genes with expression altered by immunosuppressive drug treatment may play an important role in ocular HSV-1 recurrence. Changes in expression of genes in the prostaglandin pathway, a transcription factor, and an enzyme in the cell cycle are considered especially important in HSV-1 reactivation by immunosuppression and are reviewed.
Sunday, October 19, 2008
human gene affects memory
NIH scientists have shown that a common gene variant influences memory for events in humans by altering a growth factor in the brain's memory hub. On average, people with a particular version of the gene that codes for brain derived neurotrophic factor (BDNF) performed worse on tests of episodic memory — tasks like recalling what happened yesterday. They also showed differences in activation of the hippocampus, a brain area known to mediate memory, and signs of decreased neuronal health and interconnections. These effects are likely traceable to limited movement and secretion of BDNF within cells, according to the study, which reveals how a gene affects the normal range of human memory, and confirms that BDNF affects human hippocampal function much as it does animals'.
Michael Egan, M.D., Daniel Weinberger, M.D., National Institute of Mental Health (NIMH), Bai Lu, Ph.D., National Institute of Child Health and Human Development (NICHD) and colleagues, report on their discovery in the January 24 issue of Cell.
Long known to be critical for the growth and survival of neurons, BDNF has also recently been shown to play a key role in memory and hippocampal function in animals. To find out if it works similarly in humans, the researchers explored the consequences of a tiny variance in the human BDNF gene, where its molecular makeup differs slightly across individuals. People inherit two copies of the BDNF gene — one from each parent — in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. It's called "met" because its chemical sequence contains the amino acid methionine in a location where the more common version, "val," contains valine.
"We are finding that this one amino acid substitution exerts a substantial influence on human memory, presumably because of its effects on the biology of the hippocampus," said Weinberger.
Despite its negative effect on memory, the "met" version's survival in the human genome suggests that it "may confer some compensatory advantage in other biological processes," note the researchers. Although they found that it does not confer increased susceptibility to schizophrenia, they suggest that the "met" variant might contribute to risk for — or increase functional impairment in — other disorders involving hippocampal dysfunction, such as Alzheimer's disease or mood disorders.
Drawing on participants in the NIMH intramural sibling study of schizophrenia, Egan and colleagues first assessed their hippocampal function and related it to their BDNF gene types.
Among 641 normal controls, schizophrenia patients, and their unaffected siblings, those who had inherited two copies of the "met" variant scored significantly lower than their matched peers on tests of verbal episodic (event) memory. Most notably, normal controls with two copies of "met" scored 40 percent on delayed recall, compared to 70 percent for those with two copies of "val." BDNF gene type had no significant effect on tests of other types of memory, such as semantic or working memory.
The researchers then measured brain activity in two separate groups of healthy subjects while they were performing a working memory task that normally turns off hippocampus activity. Functional magnetic resonance imaging (fMRI) scans revealed that those with one copy of "met" showed a pattern of activation along the sides of the hippocampus, in contrast to lack of activation among those with two copies of "val."
Next, an MRI scanner was used to measure levels of a marker inside neurons indicating the cell's health and abundance of synapses — tiny junctions through which neurons communicate with each other. Again, subjects with one copy of "met" had lower levels of the marker, N-acetyl-aspartate (NAA), than matched individuals with two copies of "val." Analysis showed that NAA levels dropped as the number of inherited "met" variants increased, suggesting a possible "dose effect."
Unlike other growth factors, hippocampal BDNF is secreted, in part, in response to neuronal activity, making it a likely candidate for a key role in synaptic plasticity, learning and memory. To explore possible mechanisms underlying the observed "met"- related memory effect, the researchers examined the distribution, processing and secretion of the BDNF proteins expressed by the two different gene variants within hippocampal cells. When they tagged the gene variants with green fluorescent protein and introduced them into cultured neurons, they discovered that "val" BDNF spreads throughout the cell and into the branch-like dendrites that form synapses, while "met" BDNF mostly clumps inside the cell body without being transported to the synapses. To regulate memory function, BDNF must be secreted near the synapses.
"We were surprised to see that 'met' BDNF secretion can't be properly regulated by neural activity," said Lu.
The observed memory decrements are likely traceable to the failure of "met" BDNF to reach the synapses, as well as its inability to secrete in response to neuronal activity, say the researchers.
"Our study provides direct in vivo data that the molecular mechanisms related to activity dependent BDNF secretion and signaling, such as synaptic plasticity, may underlie humans' greatly expanded verbally-mediated memory system, just as it does for more rudimentary forms of memory in animals," said Egan.
In following-up their leads, the researchers are searching for a possible BDNF connection with the memory problems and hippocampal changes of Alzheimer's disease, depression and normal aging.
Also participating in the study were: Drs. Joseph Callicott, Terry Goldberg, Bhaskar Kolachana, Alessandro Bertolino, NIMH; Drs. Masami Kojima, Eugene Zaitsev, NICHD; Dr. David Goldman, National Institute on Alcohol Abuse and Alcoholism (NIAAA); Drs. Bert Gold, Michael Dean, National Cancer Institute (NCI).
NIMH, NICHD, NIAAA and NCI are part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Graph shows the effect of BDNF gene type on performance during a test of delayed recall of memory for events among 641 participants in the NIMH Clinical Brain Disorders Branch sibling study of schizophrenia. Normal controls (heavy black line) who had inherited two copies of "met" scored 40 percent, compared to 70 percent for those with two copies of "val." Source: NIMH Clinical Brain Disorders Branch
Michael Egan, M.D., Daniel Weinberger, M.D., National Institute of Mental Health (NIMH), Bai Lu, Ph.D., National Institute of Child Health and Human Development (NICHD) and colleagues, report on their discovery in the January 24 issue of Cell.
Long known to be critical for the growth and survival of neurons, BDNF has also recently been shown to play a key role in memory and hippocampal function in animals. To find out if it works similarly in humans, the researchers explored the consequences of a tiny variance in the human BDNF gene, where its molecular makeup differs slightly across individuals. People inherit two copies of the BDNF gene — one from each parent — in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. It's called "met" because its chemical sequence contains the amino acid methionine in a location where the more common version, "val," contains valine.
"We are finding that this one amino acid substitution exerts a substantial influence on human memory, presumably because of its effects on the biology of the hippocampus," said Weinberger.
Despite its negative effect on memory, the "met" version's survival in the human genome suggests that it "may confer some compensatory advantage in other biological processes," note the researchers. Although they found that it does not confer increased susceptibility to schizophrenia, they suggest that the "met" variant might contribute to risk for — or increase functional impairment in — other disorders involving hippocampal dysfunction, such as Alzheimer's disease or mood disorders.
Drawing on participants in the NIMH intramural sibling study of schizophrenia, Egan and colleagues first assessed their hippocampal function and related it to their BDNF gene types.
Among 641 normal controls, schizophrenia patients, and their unaffected siblings, those who had inherited two copies of the "met" variant scored significantly lower than their matched peers on tests of verbal episodic (event) memory. Most notably, normal controls with two copies of "met" scored 40 percent on delayed recall, compared to 70 percent for those with two copies of "val." BDNF gene type had no significant effect on tests of other types of memory, such as semantic or working memory.
The researchers then measured brain activity in two separate groups of healthy subjects while they were performing a working memory task that normally turns off hippocampus activity. Functional magnetic resonance imaging (fMRI) scans revealed that those with one copy of "met" showed a pattern of activation along the sides of the hippocampus, in contrast to lack of activation among those with two copies of "val."
Next, an MRI scanner was used to measure levels of a marker inside neurons indicating the cell's health and abundance of synapses — tiny junctions through which neurons communicate with each other. Again, subjects with one copy of "met" had lower levels of the marker, N-acetyl-aspartate (NAA), than matched individuals with two copies of "val." Analysis showed that NAA levels dropped as the number of inherited "met" variants increased, suggesting a possible "dose effect."
Unlike other growth factors, hippocampal BDNF is secreted, in part, in response to neuronal activity, making it a likely candidate for a key role in synaptic plasticity, learning and memory. To explore possible mechanisms underlying the observed "met"- related memory effect, the researchers examined the distribution, processing and secretion of the BDNF proteins expressed by the two different gene variants within hippocampal cells. When they tagged the gene variants with green fluorescent protein and introduced them into cultured neurons, they discovered that "val" BDNF spreads throughout the cell and into the branch-like dendrites that form synapses, while "met" BDNF mostly clumps inside the cell body without being transported to the synapses. To regulate memory function, BDNF must be secreted near the synapses.
"We were surprised to see that 'met' BDNF secretion can't be properly regulated by neural activity," said Lu.
The observed memory decrements are likely traceable to the failure of "met" BDNF to reach the synapses, as well as its inability to secrete in response to neuronal activity, say the researchers.
"Our study provides direct in vivo data that the molecular mechanisms related to activity dependent BDNF secretion and signaling, such as synaptic plasticity, may underlie humans' greatly expanded verbally-mediated memory system, just as it does for more rudimentary forms of memory in animals," said Egan.
In following-up their leads, the researchers are searching for a possible BDNF connection with the memory problems and hippocampal changes of Alzheimer's disease, depression and normal aging.
Also participating in the study were: Drs. Joseph Callicott, Terry Goldberg, Bhaskar Kolachana, Alessandro Bertolino, NIMH; Drs. Masami Kojima, Eugene Zaitsev, NICHD; Dr. David Goldman, National Institute on Alcohol Abuse and Alcoholism (NIAAA); Drs. Bert Gold, Michael Dean, National Cancer Institute (NCI).
NIMH, NICHD, NIAAA and NCI are part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Graph shows the effect of BDNF gene type on performance during a test of delayed recall of memory for events among 641 participants in the NIMH Clinical Brain Disorders Branch sibling study of schizophrenia. Normal controls (heavy black line) who had inherited two copies of "met" scored 40 percent, compared to 70 percent for those with two copies of "val." Source: NIMH Clinical Brain Disorders Branch
brain activity during meditation
One basic concept of biology suggests that eukaryotic organelles arose after a primitive eukaryotic cell engulfed (swallowed, invaginated) a prokaryotic cell. This is called the endosymbiotic theory. After this invagination event, the concept continues, duplicate functions already possessed by the eukaryotic cell were eliminated, and only those prokaryotic functions that were advantageous to the eukaryotic cell were maintained. In particular, energy transduction functions, such as ATP and NADPH production, were maintained.
The two organelles that arose were the mitochondria, found in all eukoryotic cells, and chloroplasts which are found in plants and algae. Some of the genetic information of the prokaryotic cell was transferred to the nucleus of the eukaryotic cell. Chloroplast and mitochondrial sequences have been found in the nucleus of plant cells. Furthermore, chloroplast sequences have been found in the mitochondrial of plant cells. This is clear evidence that genetic control of certain biochemical functions was relinquished (or taken from) the progenitor cells. The following diagram shows the flow of genetic information from organelles in a plant cell.
It is important to note that all the basic functions of the Central Dogma of Molecular Genetics are found in organelles. This functions include DNA replication, RNA transcription and protein translation. Thus, certain gene products will result from the expression of the organelle DNA. The number of protein products from mitochondrial transcription is limited. One set of genes that are expressed are the rRNAs and tRNAs that are required for translation. Five known gene products are produced from the mammalian mitochondrial genome. These include subunits I, II and III for cytochrome oxidase, the apoprotein for cytochrome b and subunit 6 of the mitochondrial ATPase. In addition to these gene products, six ORFs have been identified. (ORF represents Open Reading Frame.) These are sequences that have transcription start and stop signals that bracket sequences that could produce a protein product, but the actual function of the product is not known. Finally, as we saw above the expression of organelle genes has a unique effect on the inheritance of certain traits.
This transfer of genetic information during the evolution of eukaryotic cells has also required the development of cooperative gene expression systems between the organelle and the nucleus. Cytochrome oxidase is one of the mitochondrial enzymes involved in ATP generation. As stated above subunits I, II, and III are encoded in the mitochondria. The remainder of the subunits of this seven subunit protein are encoded in the nucleus. The best studied example of coupled nuclear DNA/chloroplast DNA gene expression is for the protein RUBISCO (ribulose bisphoshpate carboxylase oxygenase). This is the enzyme that begins the fixation of atmospheric CO2 into sugar molecules. This enzyme has 16 subunits, eight large subunits and 8 small subunits. The large subunits are encoded by the chloroplast DNA whereas, the small subunits are encoded by nuclear DNA. Thus, for those proteins that are encoded by genes in two different cellular locations, gene expression has to be coordinated between the two locations for proper protein functioning.
Chloroplast Genomes
The chloroplast genomes of plants exhibit a far greater conversation of structure than plant mitochondrial genomes. These genomes are circular and the size of higher plant chloroplast DNAs are either *150 kb (for example, spinach) or *120 (for example pea). The difference in size can be accounted for by a deletion from the larger genome to generate the smaller. The gene order among all higher plant chloroplast genomes is essentially conserved.
As you would predict, many of chloroplast DNA genes encode proteins that are involved in photosynthesis. In total, the genome appears to encode for a complete set of rRNA and tRNA genes and *45 protein products. There are some differences between species, but these differences primarily are between higher plants and algae, which also contain chloroplast DNA.
RFLP proof that chloroplast DNA can be maternally inherited
As has been stated previously, to demonstrate that a trait is maternally inherited specific crosses need to be made to generate the required offspring. A number of crosses where made between cultivated tomato (L. esculentum) and a number of wild species. As we discussed previously, chloroplast DNA is a circular molecule *150 kb in size. Digestion of this molecule produces relatively few fragments. Within the plant cell, chloroplast DNA represents a significant portion (*15%) of the DNA. This is a result of the large number of chloroplasts per cell (*50) and the large number of chloroplast DNA molecules per chloroplast (*150).
Chloroplast DNA was obtained from F1 plants of a number of crosses in which L. esculentum was the female in the cross. As can be seen below, in each case the F1 restriction fragment pattern was identical to L. esculentum (sample 8). This is conclusive evidence that chloroplast DNA is inherited in a maternal manner. [The figures shown below are from Palmer and Zamir (1982) Proceedings of the National Academy of Science USA 79:5006.]
Mitochondrial Genomes
All of the eukaryotic species that have been analyzed to date have DNA in the mitochondria. But the size of this mitochondrial genome varies.
Size of Mitochondrial G enomes
Species |Size (kb)
--------------------------
Human | 16
Drosophila | 18
Yeast | 75
Turnip | 218
Corn | 570
Muskmelon | 2000
--------------------------
All of the mitochondrial genomes are circular. Even though there is a large size discrepancy between different species, especially between plants and animals, the number of genes that are expressed in each species is nearly the same, about 20. Thus the extra DNA that is found in the larger genomes does not appear to be required. Studies have shown that much of this DNA is in fact repeated sequences.
RFLP proof that mitochondrial DNA can be maternally inherited
Experiments designed to show that mitochondrial DNA was maternally inherited were analogous to those which demonstrated that chloroplast DNA was maternally inherited. Mouse is the experimental organism used to demonstrate this principle here. Reciprocal crosses were made between the species Mus domesticus, common mouse, and the wild species Mus spretus. F1 progeny where then backcrossed, with one of the two species serving as females. The restriction enzyme HincII is diagnostic for the mitochondrial DNA of the two species. M. domesticus mt DNA contains five restriction sites for the enzyme that generates four fragments whereas M. spretus mt DNA contains eight restriction sites which generate seven fragments. Only two of the fragments are the same size and presumably contain the same sequence information.
The figure below depicts the results of the backcross experiments. [The figure is from Gyllenstein et al. (1985) Journal of Heredity 76:321.] As you can see the female contributes the mitochondrial genome. These experiments have been repeated in other species, such as human, and the female has been shown to contribute the mitochondrial genome
The two organelles that arose were the mitochondria, found in all eukoryotic cells, and chloroplasts which are found in plants and algae. Some of the genetic information of the prokaryotic cell was transferred to the nucleus of the eukaryotic cell. Chloroplast and mitochondrial sequences have been found in the nucleus of plant cells. Furthermore, chloroplast sequences have been found in the mitochondrial of plant cells. This is clear evidence that genetic control of certain biochemical functions was relinquished (or taken from) the progenitor cells. The following diagram shows the flow of genetic information from organelles in a plant cell.
It is important to note that all the basic functions of the Central Dogma of Molecular Genetics are found in organelles. This functions include DNA replication, RNA transcription and protein translation. Thus, certain gene products will result from the expression of the organelle DNA. The number of protein products from mitochondrial transcription is limited. One set of genes that are expressed are the rRNAs and tRNAs that are required for translation. Five known gene products are produced from the mammalian mitochondrial genome. These include subunits I, II and III for cytochrome oxidase, the apoprotein for cytochrome b and subunit 6 of the mitochondrial ATPase. In addition to these gene products, six ORFs have been identified. (ORF represents Open Reading Frame.) These are sequences that have transcription start and stop signals that bracket sequences that could produce a protein product, but the actual function of the product is not known. Finally, as we saw above the expression of organelle genes has a unique effect on the inheritance of certain traits.
This transfer of genetic information during the evolution of eukaryotic cells has also required the development of cooperative gene expression systems between the organelle and the nucleus. Cytochrome oxidase is one of the mitochondrial enzymes involved in ATP generation. As stated above subunits I, II, and III are encoded in the mitochondria. The remainder of the subunits of this seven subunit protein are encoded in the nucleus. The best studied example of coupled nuclear DNA/chloroplast DNA gene expression is for the protein RUBISCO (ribulose bisphoshpate carboxylase oxygenase). This is the enzyme that begins the fixation of atmospheric CO2 into sugar molecules. This enzyme has 16 subunits, eight large subunits and 8 small subunits. The large subunits are encoded by the chloroplast DNA whereas, the small subunits are encoded by nuclear DNA. Thus, for those proteins that are encoded by genes in two different cellular locations, gene expression has to be coordinated between the two locations for proper protein functioning.
Chloroplast Genomes
The chloroplast genomes of plants exhibit a far greater conversation of structure than plant mitochondrial genomes. These genomes are circular and the size of higher plant chloroplast DNAs are either *150 kb (for example, spinach) or *120 (for example pea). The difference in size can be accounted for by a deletion from the larger genome to generate the smaller. The gene order among all higher plant chloroplast genomes is essentially conserved.
As you would predict, many of chloroplast DNA genes encode proteins that are involved in photosynthesis. In total, the genome appears to encode for a complete set of rRNA and tRNA genes and *45 protein products. There are some differences between species, but these differences primarily are between higher plants and algae, which also contain chloroplast DNA.
RFLP proof that chloroplast DNA can be maternally inherited
As has been stated previously, to demonstrate that a trait is maternally inherited specific crosses need to be made to generate the required offspring. A number of crosses where made between cultivated tomato (L. esculentum) and a number of wild species. As we discussed previously, chloroplast DNA is a circular molecule *150 kb in size. Digestion of this molecule produces relatively few fragments. Within the plant cell, chloroplast DNA represents a significant portion (*15%) of the DNA. This is a result of the large number of chloroplasts per cell (*50) and the large number of chloroplast DNA molecules per chloroplast (*150).
Chloroplast DNA was obtained from F1 plants of a number of crosses in which L. esculentum was the female in the cross. As can be seen below, in each case the F1 restriction fragment pattern was identical to L. esculentum (sample 8). This is conclusive evidence that chloroplast DNA is inherited in a maternal manner. [The figures shown below are from Palmer and Zamir (1982) Proceedings of the National Academy of Science USA 79:5006.]
Mitochondrial Genomes
All of the eukaryotic species that have been analyzed to date have DNA in the mitochondria. But the size of this mitochondrial genome varies.
Size of Mitochondrial G enomes
Species |Size (kb)
--------------------------
Human | 16
Drosophila | 18
Yeast | 75
Turnip | 218
Corn | 570
Muskmelon | 2000
--------------------------
All of the mitochondrial genomes are circular. Even though there is a large size discrepancy between different species, especially between plants and animals, the number of genes that are expressed in each species is nearly the same, about 20. Thus the extra DNA that is found in the larger genomes does not appear to be required. Studies have shown that much of this DNA is in fact repeated sequences.
RFLP proof that mitochondrial DNA can be maternally inherited
Experiments designed to show that mitochondrial DNA was maternally inherited were analogous to those which demonstrated that chloroplast DNA was maternally inherited. Mouse is the experimental organism used to demonstrate this principle here. Reciprocal crosses were made between the species Mus domesticus, common mouse, and the wild species Mus spretus. F1 progeny where then backcrossed, with one of the two species serving as females. The restriction enzyme HincII is diagnostic for the mitochondrial DNA of the two species. M. domesticus mt DNA contains five restriction sites for the enzyme that generates four fragments whereas M. spretus mt DNA contains eight restriction sites which generate seven fragments. Only two of the fragments are the same size and presumably contain the same sequence information.
The figure below depicts the results of the backcross experiments. [The figure is from Gyllenstein et al. (1985) Journal of Heredity 76:321.] As you can see the female contributes the mitochondrial genome. These experiments have been repeated in other species, such as human, and the female has been shown to contribute the mitochondrial genome
mitochondtrial dna mutation in somatic cells
Mitochondrial DNA (mtDNA) is the DNA located in organelles called mitochondria. Most other DNA present in eukaryotic organisms is found in the cell nucleus. Nuclear and mitochondrial DNA are thought to be of separate evolutionary origin, with the mtDNA being derived from the circular genomes of the bacteria that were engulfed by the early ancestors of today's eukaryotic cells. Each mitochondrion is estimated to contain 2-10 mtDNA copies.[1] In the cells of extant organisms, the vast majority of the proteins present in the mitochondria (numbering approximately 1500 different types in mammals) are coded for by nuclear DNA, but the genes for some of them, if not most, are thought to have originally been of bacterial origin, having since been transferred to the eukaryotic nucleus during evolution. Among multicellular animals (metazoans), nearly all of the mtDNA in a fertilized egg (zygote) is inherited from only one parent - the female. One mechanism for this is simple dilution: an egg contains 100,000 to 1,000,000 mitochondria, whereas a sperm contains only 10 to 100. Another mechanism, documented for a few organisms, is that the sperm mitochondria do not enter the egg. Whatever the mechanism, this single parent (uniparental) pattern of mtDNA inheritance is found in most animals, most plants and in fungi as well.
In humans (and probably in metazoans in general), 100-10,000 separate copies of mtDNA are usually present per cell (egg and sperm cells are exceptions). In mammals, each circular mtDNA molecule consists of 15,000-17,000 base pairs, which encode the same 37 genes: 13 for proteins (polypeptides), 22 for transfer RNA (tRNA) and one each for the small and large subunits of ribosomal RNA (rRNA). This pattern is also seen among most metazoans, although in some cases one or more of the 37 genes is absent and the mtDNA size range is greater. Even greater variation in mtDNA gene content and size exists among fungi and plants, although there appears to be a core subset of genes that are present in all eukaryotes (except for the few that have no mitochondria at all). Some plant species have enormous mtDNAs (as many as 2,500,000 base pairs per mtDNA molecule!) but, surprisingly, even those huge mtDNAs contain the same number and kinds of genes as related plants with much smaller mtDNAs.Contents
1 Use in identification
2 Mitochondrial inheritance
2.1 Female inheritance
2.2 Male inheritance
3 Genes
4 Genetic influence
4.1 Genetic illness
5 See also
6 References
7 External links
Use in identification
Unlike nuclear DNA, which is inherited from both parents and in which genes are rearranged in the process of recombination, there is usually no change in mtDNA from parent to offspring. Although mtDNA also recombines, it does so with copies of itself within the same mitochondrion. Because of this and because the mutation rate of animal mtDNA is higher than that of nuclear DNA,[2] mtDNA is a powerful tool for tracking ancestry through females (matrilineage) and has been used in this role to track the ancestry of many species back hundreds of generations. Human mtDNA can be used to identify individuals.[3]
Because the base sequence of animal mtDNA changes rapidly, it is useful for assessing genetic relationships of individuals or groups within a species and also for identifying and quantifying the phylogeny (evolutionary relationships; see phylogenetics) among different species, provided they are not too distantly related. To do this, biologists determine and then compare the mtDNA sequences from different individuals or species. Data from the comparisons is used to construct a network of relationships among the sequences, which provides an estimate of the relationships among the individuals or species from which the mtDNAs were taken. This approach has limits that are imposed by the rate of mtDNA sequence change. In animals, the rapid rate of change makes mtDNA most useful for comparisons of individuals within species and for comparisons of species that are closely or moderately-closely related, among which the number of sequence differences can be easily counted. As the species become more distantly related, the number of sequence differences becomes very large; changes begin to accumulate on changes until an accurate count becomes impossible.
Mitochondrial inheritance
Female inheritance
In sexually reproducing organisms, mitochondria are normally inherited exclusively from the mother. The mitochondria in mammalian sperm are usually destroyed by the egg cell after fertilization. Also, most mitochondria are present at the base of the sperm's tail, which is used for propelling the sperm cells. Sometimes the tail is lost during fertilization. In 1999 it was reported that paternal sperm mitochondria (containing mtDNA) are marked with ubiquitin to select them for later destruction inside the embryo.[4] Some in vitro fertilization techniques, particularly injecting a sperm into an oocyte, may interfere with this.
The fact that mitochondrial DNA is maternally inherited enables researchers to trace maternal lineage far back in time. (Y chromosomal DNA, paternally inherited, is used in an analogous way to trace the agnate lineage.) This is accomplished in humans by sequencing one or more of the hypervariable control regions (HVR1 or HVR2) of the mitochondrial DNA. HVR1 consists of about 440 base pairs. These 440 base pairs are then compared to the control regions of other individuals (either specific people or subjects in a database) to determine maternal lineage. Most often, the comparison is made to the revised. Vilà et al have published studies tracing the matrilineal descent of domestic dogs to wolves.[5] The concept of the Mitochondrial Eve is based on the same type of analysis, attempting to discover the origin of humanity by tracking the lineage back in time.
Because mtDNA is not highly conserved and has a rapid mutation rate, it is useful for studying the evolutionary relationships - phylogeny - of organisms. Biologists can determine and then compare mtDNA sequences among different species and use the comparisons to build an evolutionary tree for the species examined.
Male inheritance
It has been reported that mitochondria can occasionally be inherited from the father in some species such as mussels.[6][7] Paternally inherited mitochondria have also been reported in some insects such as the fruit fly[8] and the honeybee.[9]
Evidence supports rare instances of male mitochondrial inheritance in some mammals as well. Specifically, documented occurrences exist for mice,[10][11] where the male-inherited mitochondria was subsequently rejected. It has also been found in sheep,[12] and in cloned cattle.[13] It has been found in a single case in a human male and was linked to infertility.[14]
While many of these cases involve cloned embryos or subsequent rejection of the paternal mitochondria, others document in vivo inheritance and persistence under lab conditions.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Genetic influence
Genetic illness
Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome (KSS), which causes a person to lose full function of their heart, eye, and muscle movements. (See also Mitochondrial disease).
Mitochondrial disease
Human mitochondrial genetics
Paternal mtDNA transmission
Single origin theory
Mitochondrial Eve
Mitochondrial CRS
In humans (and probably in metazoans in general), 100-10,000 separate copies of mtDNA are usually present per cell (egg and sperm cells are exceptions). In mammals, each circular mtDNA molecule consists of 15,000-17,000 base pairs, which encode the same 37 genes: 13 for proteins (polypeptides), 22 for transfer RNA (tRNA) and one each for the small and large subunits of ribosomal RNA (rRNA). This pattern is also seen among most metazoans, although in some cases one or more of the 37 genes is absent and the mtDNA size range is greater. Even greater variation in mtDNA gene content and size exists among fungi and plants, although there appears to be a core subset of genes that are present in all eukaryotes (except for the few that have no mitochondria at all). Some plant species have enormous mtDNAs (as many as 2,500,000 base pairs per mtDNA molecule!) but, surprisingly, even those huge mtDNAs contain the same number and kinds of genes as related plants with much smaller mtDNAs.Contents
1 Use in identification
2 Mitochondrial inheritance
2.1 Female inheritance
2.2 Male inheritance
3 Genes
4 Genetic influence
4.1 Genetic illness
5 See also
6 References
7 External links
Use in identification
Unlike nuclear DNA, which is inherited from both parents and in which genes are rearranged in the process of recombination, there is usually no change in mtDNA from parent to offspring. Although mtDNA also recombines, it does so with copies of itself within the same mitochondrion. Because of this and because the mutation rate of animal mtDNA is higher than that of nuclear DNA,[2] mtDNA is a powerful tool for tracking ancestry through females (matrilineage) and has been used in this role to track the ancestry of many species back hundreds of generations. Human mtDNA can be used to identify individuals.[3]
Because the base sequence of animal mtDNA changes rapidly, it is useful for assessing genetic relationships of individuals or groups within a species and also for identifying and quantifying the phylogeny (evolutionary relationships; see phylogenetics) among different species, provided they are not too distantly related. To do this, biologists determine and then compare the mtDNA sequences from different individuals or species. Data from the comparisons is used to construct a network of relationships among the sequences, which provides an estimate of the relationships among the individuals or species from which the mtDNAs were taken. This approach has limits that are imposed by the rate of mtDNA sequence change. In animals, the rapid rate of change makes mtDNA most useful for comparisons of individuals within species and for comparisons of species that are closely or moderately-closely related, among which the number of sequence differences can be easily counted. As the species become more distantly related, the number of sequence differences becomes very large; changes begin to accumulate on changes until an accurate count becomes impossible.
Mitochondrial inheritance
Female inheritance
In sexually reproducing organisms, mitochondria are normally inherited exclusively from the mother. The mitochondria in mammalian sperm are usually destroyed by the egg cell after fertilization. Also, most mitochondria are present at the base of the sperm's tail, which is used for propelling the sperm cells. Sometimes the tail is lost during fertilization. In 1999 it was reported that paternal sperm mitochondria (containing mtDNA) are marked with ubiquitin to select them for later destruction inside the embryo.[4] Some in vitro fertilization techniques, particularly injecting a sperm into an oocyte, may interfere with this.
The fact that mitochondrial DNA is maternally inherited enables researchers to trace maternal lineage far back in time. (Y chromosomal DNA, paternally inherited, is used in an analogous way to trace the agnate lineage.) This is accomplished in humans by sequencing one or more of the hypervariable control regions (HVR1 or HVR2) of the mitochondrial DNA. HVR1 consists of about 440 base pairs. These 440 base pairs are then compared to the control regions of other individuals (either specific people or subjects in a database) to determine maternal lineage. Most often, the comparison is made to the revised. Vilà et al have published studies tracing the matrilineal descent of domestic dogs to wolves.[5] The concept of the Mitochondrial Eve is based on the same type of analysis, attempting to discover the origin of humanity by tracking the lineage back in time.
Because mtDNA is not highly conserved and has a rapid mutation rate, it is useful for studying the evolutionary relationships - phylogeny - of organisms. Biologists can determine and then compare mtDNA sequences among different species and use the comparisons to build an evolutionary tree for the species examined.
Male inheritance
It has been reported that mitochondria can occasionally be inherited from the father in some species such as mussels.[6][7] Paternally inherited mitochondria have also been reported in some insects such as the fruit fly[8] and the honeybee.[9]
Evidence supports rare instances of male mitochondrial inheritance in some mammals as well. Specifically, documented occurrences exist for mice,[10][11] where the male-inherited mitochondria was subsequently rejected. It has also been found in sheep,[12] and in cloned cattle.[13] It has been found in a single case in a human male and was linked to infertility.[14]
While many of these cases involve cloned embryos or subsequent rejection of the paternal mitochondria, others document in vivo inheritance and persistence under lab conditions.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Genetic influence
Genetic illness
Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome (KSS), which causes a person to lose full function of their heart, eye, and muscle movements. (See also Mitochondrial disease).
Mitochondrial disease
Human mitochondrial genetics
Paternal mtDNA transmission
Single origin theory
Mitochondrial Eve
Mitochondrial CRS
to study the patterning of memory in human brain
Aim:
To study the patterning of memory in human brain
Theory:
The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability of storing data in human brain artificially. The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability
To study the patterning of memory in human brain
Theory:
The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability of storing data in human brain artificially. The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability
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