ScienceDaily (May 10, 2012) — Researchers at the Medical Research Council (MRC) Toxicology Unit at the University of Leicester have identified a major pathway leading to brain cell death in mice with neurodegenerative disease. The team was able to block the pathway, preventing brain cell death and increasing survival in the mice.

Scientists have identified a major pathway leading to brain cell death in mice with neurodegenerative disease. The team was able to block the pathway, preventing brain cell death and increasing survival in the mice. (Credit: © pressmaster / Fotolia)

In human neurodegenerative diseases, including Alzheimer’s, Parkinson’s and prion diseases, proteins “mis-fold” in a variety of different ways resulting in the build up of mis-shapen proteins. These form the plaques found in Alzheimer’s and the Lewy bodies found in Parkinson’s disease.

The researchers studied mice with neurodegeneration caused by prion disease. These mouse models currently provide the best animal representation of human neurodegenerative disorders, where it is known that the build up of mis-shapen proteins is linked with brain cell death.

They found that the build up of mis-folded proteins in the brains of these mice activates a natural defense mechanism in cells, which switches off the production of new proteins. This would normally switch back ‘on’ again, but in these mice the continued build-up of mis-shapen protein keeps the switch turned ‘off’. This is the trigger point leading to brain cell death, as those key proteins essential for nerve cell survival are not made.

By injecting a protein that blocks the ‘off’ switch of the pathway, the scientists were able to restore protein production, independently of the build up of mis-shapen proteins,and halt the neurodegeneration. The brain cells were protected, protein levels and synaptic transmission (the way in which brain cells signal to each other) were restored and the mice lived longer, even though only a very small part of their brain had been treated.

Mis-shapen proteins in human neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases, also over-activate this fundamental pathway controlling protein synthesis in the brains of patients, which represents a common target underlying these different clinical conditions. The scientists’ results suggest that treatments focused on this pathway could be protective in a range of neurodegenerative disease in which mis-shapen proteins are building up and causing neurons to die.

Professor Giovanna Mallucci, who led the team, said, “What’s exciting is the emergence of a common mechanism of brain cell death, across a range of different neurodegenerative disorders, activated by the different mis-folded proteins in each disease. The fact that, in mice with prion disease, we were able to manipulate this mechanism and protect the brain cells means we may have a way forward in how we treat other disorders. Instead of targeting individual mis-folded proteins in different neurodegenerative diseases, we may be able to target the shared pathways and rescue brain cell degeneration irrespective of the underlying disease.”

Professor Hugh Perry, chair of the MRC’s Neuroscience and Mental Health Board, said, “Neurodegenerative diseases such as Alzheimer’s and Parkinson’s are debilitating and largely untreatable conditions. Alzheimer’s disease and related disorders affect over seven million people in Europe, and this figure is expected to double every 20 years as the population ages across Europe. The MRC believes that research such as this, which looks at the fundamental mechanisms of these devastating diseases, is absolutely vital. Understanding the mechanism that leads to neuronal dysfunction prior to neuronal loss is a critical step in finding ways to arrest disease progression.”

Source: Science Daily

May 10th, 2012

Glial cells pass on metabolites to neurons.

Around 100 billion neurons in the human brain enable us to think, feel and act. They transmit electrical impulses to remote parts of the brain and body via long nerve fibres known as axons. This communication requires enormous amounts of energy, which the neurons are thought to generate from sugar. Axons are closely associated with glial cells which, on the one hand, surround them with an electrically insulating myelin sheath and, on the other hand support their long-term function. Klaus Armin and his research group from the Max Planck Institute of Experimental Medicine in Göttingen have now discovered a possible mechanisms by which these glial cells in the brain can support their associated axons and keep them alive in the long term.

Oligodendrocytes are a group of highly specialised glial cells in the central nervous system. They are responsible for the formation of the fat-rich myelin sheath that surrounds the nerve fibres as an insulating layer. The comparison with the coating on electricity cables is an obvious one; however, myelin can do much more than act as the insulating layer on electricity cables: it increases the transmission speed of the axons and also reduces ongoing energy consumption. The extreme importance of myelin for a functioning nervous system is shown by the diseases that arise from a defective insulating layer, such as multiple sclerosis

Interestingly, the function of the oligodendrocytes goes far beyond the mere provision of myelin. Klaus-Armin Nave and his team at the Max Planck Institute in Göttingen already succeeded in demonstrating years ago that healthy glial cells are also essential for the long-term function and survival of the axons themselves, irrespective of myelination. “The way in which the oligodendrocytes functionally support their associated axons was not clear to us up to now,” says Nave. In a new study, the researchers were able to show that the glial cells are involved in, among other things, the replenishment of energy in the nerve fibres. “They could be described as the petrol stations on the data highway of the axons,” says Nave, explaining the results.

Electron microscope cross-section image of the nerve fibres (axons) of the optic nerve. Axons are surrounded by special glial cells, the oligodendrocytes, wrapping themselves around the axons in several layers. Between the axons, there are extensions of astrocytes, another type of glial cells. © K.-A.Nave/MPI f. Experimental Medicine

But how does the energy refuelling work? Is there a metabolic connection between the oligodendrocytes and axons? To find out, Ursula Fünfschilling generated genetically modified mice: the function of the mitochondria was deliberately disrupted in the oligodendrocytes through the inactivation of the Cox10 gene. This affects the final stages of sugar breakdown taking place in the mitochondria where energy is harnessed – a process known as the respiratory chain. If a link in this chain is missing, in this instance cytochrome oxidase, which is only functional when cells have the enzyme Cox10, the glial cells gradually lose the capacity for cell respiration in their mitochondria. “Without independent breathing, the manipulated glial cells of the nervous systems should have died,” explains the scientist. That is, unless the low level of energy harnessed from the splitting of the glucose to form pyruvate or milk acid, a process known as glycolysis, is sufficient for them.

And this is precisely what the scientists observed in their mice: the animals’ myelin was initially formed in the normal way. The loss of the mitochondrial respiratory chain, which started at this point, did not appear to affect the glial cells in the central nervous system. Even one year later, there were no neurodegenerative changes in the brain to be observed. The scientists assume that in the early weeks of life – a phase characterised by maximum energy requirement – the mutated oligodendrocytes still rely on many intact mitochondria. All of the more mature oligodendrocytes later appear to reduce the mitochondrial respiration and set it to energy generation through increased glycolysis. This has the advantage in healthy glial cells that the metabolic products which arise during the breaking down of glucose can be used as components for myelin synthesis. In addition, the lactic acid that arises in the oligodendrocytes can be given to the axons where it can be used to produce energy with the help of the axon’s own mitochondria.

“The complete loss of the respiratory chain in the deliberately modified oligodendrocytes probably elevates a developmental step that unfolds naturally,” explains Nave. Thus the loss of glial mitochondria does not result in the deterioration of the energy supply to the axons but, conversely, to an oversupply of exploitable lactic acid. The affected nerve pathways themselves have no problem demonstrably in metabolising the lactic acid from oligodendrocytes. Transport proteins ensure the rapid transfer of the lactic acid between the oligodendrocytes and their myelinated axons.

This finding provides a new understanding of the role of oligodendrocytes: in addition to their known significance for myelinisation [aka myelination], they can directly provide the axons with glucose products that can be used as fuel with the help of axonal mitochondria in periods of high activity. This coupling of glial cells could explain, among other things, why in many myelin diseases, for example multiple sclerosis, the affected demyelinised axons often suffer irreversible damage.

Source: Neuroscience News

ScienceDaily (May 10, 2012) — Research into hearing loss after exposure to loud noises could lead to the first drug treatments to prevent the development of tinnitus.

Researchers in the University of Leicester’s Department of Cell Physiology and Pharmacology have identified a cellular mechanism that could underlie the development of tinnitus following exposure to loud noises. The discovery could lead to novel tinnitus treatments, and investigations into potential drugs to prevent tinnitus are currently underway.

Tinnitus is a sensation of phantom sounds, usually ringing or buzzing, heard in the ears when no external noise is present. It commonly develops after exposure to loud noises (acoustic over-exposure), and scientists have speculated that it results from damage to nerve cells connected to the ears.

Although hearing loss and tinnitus affect around ten percent of the population, there are currently no drugs available to treat or prevent tinnitus.

University of Leicester researcher Dr Martine Hamann, who led the study published in the journal Hearing Research, said: “We need to know the implications of acoustic over exposure, not only in terms of hearing loss but also what’s happening in the brain and central nervous system. It’s believed that tinnitus results from changes in excitability in cells in the brain — cells become more reactive, in this case more reactive to an unknown sound.”

Dr Hamann and her team, including PhD student Nadia Pilati, looked at cells in an area of the brain called the dorsal cochlear nucleus — the relay carrying signals from nerve cells in the ear to the parts of the brain that decode and make sense of sounds. Following exposure to loud noises, some of the nerve cells (neurons) in the dorsal cochlear nucleus start to fire erratically, and this uncontrolled activity eventually leads to tinnitus.

Dr Hamann said “We showed that exposure to loud sound triggers hearing loss a few days after the exposure to the sound. It also triggers this uncontrolled activity in the neurons of the dorsal cochlear nucleus. This is all happening very quickly, in a matter of days”

In a key breakthrough in collaboration with GSK who sponsored Dr Pilati’s PhD, the team also discovered the specific cellular mechanism that leads to the neurons’ over-activity. Malfunctions in specific potassium channels that help regulate the nerve cell’s electrical activity mean the neurons cannot return to an equilibrium resting state.

Ordinarily, these cells only fire regularly and therefore regularly return to a rest state. However, if the potassium channels are not working properly, the cells cannot return to a rest state and instead fire continuously in random bursts, creating the sensation of constant noise when none exists.

Dr Hamann explained: “In normal conditions the channel helps to drag down the cellular electrical activity to its resting state and this allows the cell to function with a regular pattern. After exposure to loud sound, the channel is functioning less and therefore the cell is constantly active, being unable to reach its resting state and displaying those irregular bursts.”

Although many researchers have investigated the mechanisms underlying tinnitus, this is the first time that cellular bursting activity has been characterised and linked to specific potassium channels. Identifying the potassium channels involved in the early stages of tinnitus opens up new possibilities for preventing tinnitus with early drug treatments.

Dr Hamann’s team is currently investigating potential drugs that could regulate the damaged cells, preventing their erratic firing and returning them to a resting state. If suitable drug compounds are discovered, they could be given to patients who have been exposed to loud noises to protect them against the onset of tinnitus.

These investigations are still in the preliminary stages, and any drug treatment would still be years away.

Source: Science Daily

ScienceDaily (May 10, 2012) — By comparing the testosterone levels of five-month old pairs of twins, both identical and non-identical, University of Montreal researchers were able to establish that testosterone levels in infancy are not inherited genetically but rather determined by environmental factors.

Angry boy. Testosterone levels in infancy are not inherited genetically but rather determined by environmental factors, new research suggests. (Credit: © crestajohnson / Fotolia)

"Testosterone is a key hormone for the development of male reproductive organs, and it is also associated with behavioural traits, such as sexual behaviour and aggression," said lead author Dr. Richard E. Tremblay of the university’s Research Unit on Children’s Psychosocial Maladjustment. "Our study is the largest to be undertaken with newborns, and our results contrast with the findings gained by scientists working with adolescents and adults, indicating that testosterone levels are inherited."

The findings were presented in an article published inPsychoneuroendocrinology on May 7, 2012.

The researchers took saliva samples from 314 pairs of twins and measured the levels of testosterone. They then compared the similarity in testosterone levels between identical and fraternal twins to determine the contribution of genetic and environmental factors. Results indicated that differences in levels of testosterone were due mainly to environmental factors. “The study was not designed to specifically identify these environmental factors which could include a variety of environmental conditions, such as maternal diet, maternal smoking, breastfeeding and parent-child interactions.”

"Because our study suggests that testosterone levels in infants are determined by the circumstances in which the child develops before and after birth, further studies will be needed to find out exactly what these influencing factors are and to what extent they change from birth to puberty," Tremblay said.

Source: Science Daily

May 10th, 2012

A recently evolved pattern of gene activity in the language and decision-making centers of the human brain is missing in a disorder associated with autism and learning disabilities, a new study by Yale University researchers shows.

“This is the cost of being human,” said Nenad Sestan, associate professor of neurobiology, researcher at Yale’s Kavli Institute for Neuroscience, and senior author of the paper. “The same evolutionary mechanisms that may have gifted our species with amazing cognitive abilities have also made us more susceptible to psychiatric disorders such as autism.”

The findings are reported in the May 11 issue of the journal Cell.

In the Cell paper, Kenneth Kwan, the lead author, and other members of the Sestan laboratory identified the evolutionary changes that led the NOS1 gene to become active specifically in the parts of the developing human brain that form the adult centers for speech and language and decision-making. This pattern of NOS1 activity is controlled by a protein called FMRP and is missing in Fragile X syndrome, a disorder caused by a genetic defect on the X chromosome that disrupts FMRP production. Fragile X syndrome, the leading inherited form of intellectual disability, is also the most common single-gene cause of autism. The loss of NOS1 activity may contribute to some of the many cognitive deficits suffered by those with Fragile X syndrome, such as lower IQ, attention deficits, and speech and language delays, the authors say.

The pattern of NOS1 activity in these brain centers does not occur in the developing mouse brain — suggesting that it is a more recent evolutionary adaptation possibly involved in the wiring of neural circuits important for higher cognitive abilities. The findings of the Cell paper support this hypothesis. The study also provides insights into how genetic deficits in early development, a time when brain circuits are formed, can lead to disorders such as autism, in which symptoms appear after birth.

“This is an example of where the function of genetic changes that likely drove aspects of human brain evolution was disrupted in disease, possibly reverting some of our newly acquired cognitive abilities and thus contributing to a psychiatric outcome,” Kwan said.

Artist representation of early developmental brain cells that when disrupted cause Fragile X syndrome. Adapted from Yale University press release image.

By Bill Hathaway

Source: Neuroscience News

May 10, 2012

Scientists have confirmed that mutations of a gene are responsible for some cases of a rare, inherited disease that causes progressive muscle degeneration and weakness: spinal muscular atrophy with lower extremity predominance, also known as SMA-LED.

"Typical spinal muscular atrophies begin in infancy or early childhood and are fatal, involving all motor neurons, but SMA-LED predominantly affects nerve cells controlling muscles of the legs. It is not fatal and the prognosis is good, although patients usually are moderately disabled and require assistive devices such as bracing and wheelchairs throughout their lives," said Robert H. Baloh, MD, PhD, director of Cedars-Sinai Medical Center’s Neuromuscular Division and senior author of a Neurology article describing the new findings on DYNC1H1.

It is a molecule inside cells that acts as a motor to transport cellular components. Using cells cultured from patients, Baloh’s group showed that the mutation disrupts this motor’s function. The researchers found that some subjects with mutations had global developmental delay in addition to weakness, indicating the brain also is involved.

"Our observations suggest that a range of DYNC1H1-related disease exists in humans – from a widespread neurodevelopmental abnormality of the central nervous system to more selective involvement of certain motor neurons, which manifests as spinal muscular atrophy," Baloh said.

He pointed out that while this molecule is responsible for some inheritable cases of spinal muscular atrophy with lower extremity predominance, the genetic mutation is absent in others. The search continues, therefore, to find other culprit genetic mutations and develop biological therapies to correct them.

"Although this is a rare form of motor neuron disease, it tells us that dynein function – the molecular motor – is crucial for the development and maintenance of motor neurons, which we hope will provide insight into the common form of spinal muscular atrophy and also amyotrophic lateral sclerosis," Baloh said. ALS (also known as Lou Gehrig’s disease) is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord.

Baloh, an expert in treating and studying neuromuscular and neurodegenerative diseases, joined Cedars-Sinai in early 2012, working with other physicians and scientists in the Department of Neurology and the Regenerative Medicine Institute to establish one of the most comprehensive neuromuscular disease treatment and research teams in California.

Provided by Cedars-Sinai Medical Center

Source: medicalxpress.com

May 10, 2012

(Medical Xpress) — A new mathematical model predicting how nerve fibres make connections during brain development could aid understanding of how some cognitive disorders occur.

The model, constructed by scientists at the Queensland Brain Institute (QBI) and School of Mathematics and Physics at the University of Queensland (UQ), gives new insight into how changing chemical levels in nerve fibres can modify nerve wiring underpinning connections in the brain.

Professor Geoff Goodhill says that while scientists have long known that changing these chemical levels can change where nerve fibres grow, only now are they understanding why this is the case.

“Our mathematical model allows us to predict precisely how these chemical levels control the direction in which nerve fibres grow, during both neural development and regeneration after injury,” he said.

Correct brain wiring is fundamental for normal brain function.

Recent discoveries suggest that wiring problems may underpin a number of nervous system disorders including autism, dyslexia, Down syndrome, Tourette’s syndrome and Parkinson’s disease.

The new model, published in the prestigious cell journal Neurondemonstrates the important role mathematics can play in understanding how the brain develops, and perhaps ultimately preventing such disorders. 

Provided by University of Queensland 

Source: medicalxpress.com

May 10, 2012

(Medical Xpress) — Scientists at University of Queensland’s Brain Institute are one step closer to developing new therapies for treating dementia.

QBI’s Dr Jana Vukovic said the work was aimed at understanding the molecular mechanism that may impair learning and memory in the ageing population.

“Ageing slows the production of new nerve cells, reducing the brain’s ability to form new memories,” said Dr Vokovic, who performed the work in the laboratory of Professor Perry Bartlett, the Director of QBI at The University of Queensland.

"But our research shows for the first time that the brain cells usually responsible for mediating immunity, microglia, have an inhibitory effect on memory during ageing.

“Furthermore, they have shown that a molecule produced by nerve cells, fractalkine, can reverse this process and stimulate stem cells to produce new neurons.”

The discovery, published in The Journal of Neuroscience today, came after QBI scientists observed that the increased production of new neurons in mice that were actively running was due to the release of fractalkine in the hippocampus – the brain structure responsible for specific types of learning and memory.

Professor Bartlett said it had been known for some time that exercise increased the production of new nerve cells in the hippocampus in young and even aged mice.

“But this study found that it is fractalkine that appears to be specifically mediating this effect by making the microglia produce factors that activate the stem cells that produce new nerve cells,” he said.

“Once the cells are activated they divide and produce new cells, which underpin the animal’s ability to learn and form memories.

"This means that fractalkine may form the basis for the development of future therapies.

“The discovery is especially exciting because we have found that older animals suffering cognitive decline showed significantly lower levels of fractalkine.

“We are seeking ways of increasing fractalkine levels in patients with cognitive decline, and hoping this may be a new frontline therapy in treating dementia.”

Dr Vukovic said that until relatively recently, it was thought the adult brain was incapable of generating new neurons.

“But work from Professor Bartlett’s laboratory over the past 20 years has demonstrated that the brains of adult animals, including humans, retain the ability to make new nerve cells,” she said.

“The challenge is to find out how to stimulate this production in the aged animal and human where production has slowed.”

The latest work was a significant step toward achieving this goal, she said.

Provided by University of Queensland

Source: medicalxpress.com

May 10, 2012

(Medical Xpress) — How do we build a memory in the brain? It is well known that for animals (and humans) new proteins are needed to establish long-term memories. During learning information is stored at the synapses, the junctions connecting nerve cells. Synapses also require new proteins in order to show changes in their strength (synaptic plasticity). Historically, scientists have focused on the cell body as the place where the required proteins are synthesized. However, in recent years there has been increasing focus on the dendrites and axons (the compartments that meet to form synapses) as a potential site for protein synthesis.

Protein synthesis machines have been observed there as well as a limited number of their templates, the messenger RNA molecules. The limited number of mRNAs observed in dendrites and axons placed constraints on the constellation of proteins that could be synthesized to help synapses work and change. Researchers from Erin Schuman’s lab at the Max Planck Institute (MPI) for Brain Research used new-generation sequencing to directly identify a very large number (over 2500) of new mRNA molecules that are present at the axons and dendrites. Using high-resolution imaging techniques they were able to both quantify and visualize individual mRNA molecules. They published their findings in the latest issue of Neuron.

[Video]
Erin Schuman and her colleagues describe how they were able to detect numerous new mRNAs in the processes of neurons with unprecedented sensitivity. Video: Neuron.

Using microarray approaches and/or in situ hybridization techniques, many different groups had each identified a hundred or so mRNAs that might reside in the dendrites. By analyzing and comparing these studies the Schuman team discovered something surprising: it seems that not a single mRNA type was found in all three studies. This observation made the scientist at the MPI for Brain Research wonder whether the already discovered mRNAs are just the tip of the iceberg and whether there were many more mRNA molecules waiting to be discovered.

In order to find out the researchers dissected the neuropil layer of the rat hippocampus. This layer comprises a high concentration of axons and dendrites, but lacks the cell bodies of pyramidal neurons (the principal cell type in the hippocampus and other brain areas). By using sensitive high-resolution sequencing techniques, mRNAs could be detected which, due to their lower concentrations, were not discovered before. The researchers found an impressive number of 2550 unique mRNAs present at the dendrites and/or axons. To determine the relative abundance in the neuronal cells, the scientists at Erin Schuman’s lab used the Nanostring nCounter, a new technique allowing the high-resolution visualization and quantification of single mRNA molecules. They found that the concentration of mRNAs in the euronal cells varies by three orders of magnitude. Additionally, the researchers were able to classify many of the mRNAs and determine their function in synaptic plasticity. These include signaling molecules, scaffolds and the receptors for neurotransmitter molecules. In addition, many mRNAs coding for protein implicated in diseases like autism were discovered in the dendrites and axons. Finally, by using advanced imaging techniques, the researchers could directly visualize some of the mRNAs in the neuronal dendrites, hundreds of micrometers from the cell body.

These results reveal a previously unappreciated enormous potential for the local protein synthesis machinery to supply, maintain and modify the dendritic and synaptic protein population. It seems that neurons use a local control mechanism much in the same way that modern societies have learned that the most efficient means to distribute goods to the population is to use local distribution centers.

Provided by Max Planck Society

Source: medicalxpress.com

May 9, 2012 

Efforts to understand how the aging process affects the brain and cognition have expanded beyond simply comparing younger and older adults.

"Everybody ages differently. By looking at genetic variations and individual differences in markers of vascular health, we begin to understand that preventable factors may affect our chances for successful aging," said Wayne State University psychology doctoral student Andrew Bender, lead author of a study supported by the National Institute on Aging of the National Institutes of Health and now in press in the journal Neuropsychologia.

The report, “Age-related Differences in Memory and Executive Functions in Healthy APOE ε4 Carriers: The Contribution of Individual Differences in Prefrontal Volumes and Systolic Blood Pressure,” focuses on carriers of the ε4 variant of the apolipoprotein (APOE) gene, present in roughly 25 percent of the population. Compared to those who possess other forms of the APOE gene, carriers of the ε4 allele are at significantly greater risk for Alzheimer’s, dementia and cardiovascular disease.

Many studies also have shown that nondemented carriers of the APOE ε4 variant have smaller brain volumes and perform less well on cognitive tests than carriers of other gene variants. Those findings, however, are not consistent, and a possible explanation may come from examining interactions between the risky genes and other factors, such as markers of cardiovascular health. Prior research in typical samples of older adults has shown that indeed other vascular risk factors — such as elevated cholesterol, hypertension or diabetes — can exacerbate the impact of the APOE ε4 variant on brain and cognition, but it is unclear if such synergy of risks is present in healthy adults.

Thus, Wayne State researchers evaluated a group of volunteers from 19 to 77 years of age who self-reported as exceptionally healthy on a questionnaire that screened for a number of conditions, representing a “best case scenario” of healthy aging. The research project, led by Naftali Raz, Ph.D., professor of psychology and director of the Lifespan Cognitive Neuroscience Research Program at WSU’s Institute of Gerontology, tested different cognitive abilities known for their sensitivity to aging and the effects of the APOE ε4 variant. Those abilities include speed of information processing, working memory (holding and manipulating information in one’s mind) and episodic memory (memory for events).

Researchers also measured participants’ blood pressure, performed genetic testing to determine which APOE variant participants carried, and measured the volumes of several critical brain regions using a high-resolution structural magnetic resonance imaging brain scan. Bender and Raz showed that for older APOE ε4 carriers, even minor increases in systolic blood pressure (the higher of the two numbers that are reported in blood pressure measures) were linked with smaller volumes of the prefrontal cortex and prefrontal white matter, slower speed of information processing, reduced working memory capacity and worse verbal memory. Notably, they said, that pattern was not evident in those who lacked the ε4 gene variant.

The study concludes that the APOE ε4 gene may make its carriers sensitive to negative effects of relatively subtle elevations in systolic blood pressure, and that the interplay between two risk factors, genetic and physiological, is detrimental to the key brain structures and associated cognitive functions.

"Although genes play a significant role in shaping the effects of age and vascular risk on the brain and cognition, the impact of single genetic variants is relatively small, and there are quite a few of them. Thus, one’s aging should not be seen through the lens of one’s genetic profile," cautioned the study’s authors. They continued, "The negative impact of many genetic variations needs help from other risk factors, and while there isn’t much one can do about genes, a lot can be done about vascular risk factors such as blood pressure or cholesterol."

"Everybody should try to keep those in check, although people with certain genetic variants more so than others." Raz said. "Practically speaking, even with the best deck of genetic cards dealt to you, it still makes sense to reduce risk through whatever works: exercise, diet or, if those fail, medication."

Because the study is part of a longitudinal project, he and Bender said the immediate future task now is to determine how the interaction between risky genes and vascular risk factors affect the trajectory of age-related changes — not differences, as in this cross-sectional study — in brain and cognition.

Provided by Wayne State University

Source: medicalxpress.com