BRAIN TRANSPLANT LETS RECORDED MEMORIES BE PLAYED BACK

A study, published in the journal Science, shows that brain transplants in a key area of mice brains is more repairable than was widely believed. No development in this area was bigger than an implant designed to record and replay memories.

In this study, neuronal transplants have repaired brain circuitry and normalized function in mice with a brain disorder, being unable to respond to leptin, a hormone that regulates metabolism and controls body weight.

These mutant mice usually become morbidly obese, but the neuron transplants repaired defective brain circuits, letting them to respond to leptin and gain much less weight.

Performing a memory task that trained a group of implant rats to get a drink of water by touching one lever in a cage, then—after a distraction—touching another. In order to know which lever to push the second time, they had to remember which one they’d already pushed. Electrodes in the implants recorded signals between two areas of their brains involved in storing new information in long-term memory. Researchers gave the rats a drug that kept those brain areas from communicating.

The rats still knew they had to press one lever then the other to get water, but couldn’t remember which lever they’d already pressed. When researchers played back the neural signals they’d recorded earlier via the implants, the rats again remembered which lever they had hit, and pressed the other one. When researchers played back the signals in rats not on the drug (thus amplifying their normal memory) the rats made fewer mistakes and remembered which lever they’d pressed even longer.

The study found that newly developed neurons from embryonic cells are efficient at integrating with the native neuronal circuitry. They communicated to recipient neurons through normal synaptic contacts, and that the brain, in turn, signaled back. Responding to leptin, insulin and glucose, these neurons had effectively joined the brain’s network and rewired the damaged circuitry.

This ground-breaking research shows that neural signals involved in memory can be recorded and replayed, suggesting the possibility of new therapeutic approaches to conditions such as spinal cord injury, autism, epilepsy, ALS (Lou Gehrig’s disease), Parkinson’s disease, Huntington’s disease and dementias such as Alzheimer’s disease.

Posted in Alzheimer's Disease, Brain Injury, How the Brain Works, How the Memory Works, Neuroplasticity, neuroscience, Stroke, Uncategorized | View Comments

Nicotine Patch Reduced Early Memory Loss In MCI Study

The same nicotine found in cigarettes is chemically similar to acetylcholine, a natural chemical in the brain associated with memory performance. When acetylcholine levels are reduced due to certain conditions such as Alzheimer’s disease (AD), memory performance is also reduced.

That may explain the findings of a study published in Neurology that a nicotine patch helped improve the memory performance of people with mild cognitive impairment (MCI), a likely pre-curser of AD, versus people on a plecebo patch. Memory performance of those on placebo stayed the same or got worse. This research suggests that nicotine may also help improve attention and mental processing in addition to memory.

This modest 6 month study – involving 70 people over age 55 – is the largest trial ever performed looking at how nicotine might improve memory. Researchers explain that nicotine actually mimics the neurotransmitter acetylcholine, which stimulates nerve cell receptors in the brain. Stimulating these receptors revs up the system involved in attention, learning and memory skills.
This helps explain why when smokers quit and cut their nicotine intake to zero, they may have a harder time remembering things. Eventually, their brains rebound and memory returns to normal if the person’s memory function is normal and not impaired by MCI.

The study did not show a significant change in subjects’ ability to handle life’s everyday problems, despite nicotine improving their memory somewhat.

While subjects suffered no serious side effects and had no trouble discontinuing the treatment, all thoughts of using a nicotine patch should be discussed with your physician or health provider first.
A larger and longer trial to more fully determine the effect of nicotine therapy on the trajectory of how people decline in dementia.

Posted in AD Drug Research, Alzheimer's Disease, How the Brain Works, How the Memory Works, Memory Health, neuroscience, Uncategorized | View Comments

TO MAINTAIN MEMORY FITNESS REMEMBER VITAMIN B EVERY DAY

Science tells us that vitamin B helps maintain healthy nerve cells and red blood cells. A vitamin B-12 deficiency — most common in older adults and vegetarians — can cause various signs and symptoms, including memory loss. In such cases, vitamin B-12 supplements can help improve memory performance.

A daily dose of B vitamins and folic acid can dramatically combat memory loss in old age and even protect against Alzheimer’s, a study published in the International Journal of Geriatric Psychiatry reported. People taking vitamin B supplements had lower levels of the blood amino acid homocysteine known to lead to a rise in the risk of dementia. Studies found that vitamin B also slowed mental decline in older people who have slight problems with their memory.

The Oxford University study of more than 250 people, aged 70 years or older, including people with mild cognitive impairment – a precursor to Alzheimer’s disease – were given a natural form of vitamin B-12 found in beans, meat, whole grains and bananas – or a placebo – over a two-year period.

Taking the food supplement appeared to help maintain mental processes, such as planning, organizing and recalling information. An earlier study showed B vitamins (12, 6 and folic acid) slowed the rate of brain shrinkage compared with a group receiving a placebo.

In the absence of a vitamin B-12 deficiency, there are no peer-reviewed studies to substantiate that vitamin B-12 supplements enhance memory for people who have Alzheimer’s disease. Still, vitamin B-12 remains an important part of a healthy diet and maintenance of lifespan memory fitness.

If you’re concerned that you’re not getting enough vitamin B-12 or other specific nutrients, consult your doctor — especially if you’re an older adult or a vegetarian.

Posted in Alzheimer's Disease, How the Brain Works, How the Memory Works, Memory Fitness, Memory Health, neuroscience, Uncategorized | View Comments

Epigentics And Neuroplastcity Share Brain Development From The Start.

A study published in the journal Neuron, illustrates the effect of environmental inputs (epigentics) on the developing brain’s neuroplasticity. Exposure to just 20 minutes of intensive visual stimulation during the brain’s development led to enhanced visual acuity and higher sensitivity to finer and smaller visual targets than non-conditioned controls.

Using time-lapse imaging to follow changes in developmental brain circuitry, researchers studying the network of connections between nerve cells (wiring) found the brain’s dynamic neuronal connections and networks are plastic —changing and adapting to the demands of the environment. Many brain diseases are thought to result from errors in brain wiring due to a disruption of the complex interactions between genetic and epigenetic environmental influences during early neuroplastic brain development.

From birth to about 3-5 years of age, an initial overproduction of general or non-specific connections between nerve cells, typically about twice as many as needed. During developmental learning many general connections – about half -are pruned, leaving only those that are strong and specific.

Research shows that exposure to enriched environments with extra sensory and social stimulation enhances the connectivity of the synapses, but children and adolescents can lose them – up to 20 million per day – when not stimulated. For example, hearing spoken language from birth stimulates neuronal connections for correct pronunciation. Adult language learners speaking with an accent do so because their developing brains did not actually hear specific ‘foreign’ sounds. That’s why teaching a languages before the age of 5 is so effective.

This study focused on environmental stimulation from intense visual stimulation on refinement and enhancement of neuronal receptivity for visual acuity (clearness of vision due to sharpness of retinal focus).

Research such as this is advancing knowledge about neuroplasticity (changes in networks) and epigenetics (effects of environmental factors) on how the brain develops is vital to finding advanced therapies, treatments and even early intervention, especially for developmental disorders such as autism and attention deficit hyperactivity disorder (ADHD).

Additional research seeking advanced treatments for injuries to the brain from traumatic brain injury and stroke, as well as therapies for developmental disorders, is ongoing.

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Brain Imaging Shows Signs of Attention Deficit

Attention deficit hyperactivity disorder (ADHD) is not just for kids. In an effort to identify ADHD early in the course of the diagnosis, researchers at the Kennedy Krieger Institute examined the brains of young children to determine if early intervention could aid long-term outcomes.

The researchers found that preschool children with early symptoms of attention deficit hyperactivity disorder (ADHD) show differences in their brain development. Characterized by inattentiveness, hyperactivity and impulsivity, ADHD affects more than 2 million US children and adults and is the most common pediatric behavioral diagnosis. By age 4, as many as 40 % of children are at risk for exhibiting attention problems of concern to parents and preschool teachers.

Insights into brain differences associated with ADHD were gained from earlier magnetic resonance imaging (MRI) studies focused on children ages 7 and older.

In this study, researchers examined brain images in 4-5 year old preschoolers, both with and without ADHD symptoms, looking at cortical and basal ganglia size and volume. Analysis of high resolution MRI brain images of 26 preschoolers, half with ADHD symptoms, found differences in the caudate nucleus, a small subcortical brain structure associated with cognitive and motor control.
Data analysis revealed three things: that children with ADHD symptoms had significantly reduced caudate volumes; that caudate volumes were significantly correlated with parent ratings of hyperactive/impulse control symptoms; and, that symptom severity did not correlate with cortical volumes.

Researchers, concluding that differences in development of basal ganglia in the caudate nucleus appear to play an important role among children presenting with early symptoms of ADHD, will continue to follow the brain development of the targeted children to determine if abnormalities persist – or regress – on aging. If they do persist, research could lead to early interventions and perhaps prevention.

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Manage Your Blood Sugar to Reduce Diabetes and Alzheimer’s Risks

Two serious healthcare trends – the soaring rates of 1) Type 2 diabetes and 2) dementia – have biological factors in common, which scientists are beginning to believe is more than coincidental.

An estimated 10% of dementia cases may be attributable to diabetes and, according to researchers knowledgeable on the relationship between the diseases, treating diabetes and risk factors linked to it, such as hypertension and high cholesterol, may help prevent many dementia cases, especially because hypertension and high cholesterol could trigger the dementia process years before symptoms of memory loss occur.

In fact, it is now thought that control of blood sugar level could pay off by reducing the number of people at risk for Alzheimer’s disease, other forms of dementia and even normal age-related cognitive decline.

According to the Alzheimer’s Association, the clogged arteries and inflammation in cells found in the development of heart disease and stroke also affect the brain. Therefore, reduction of diabetes risk is also good for reduction of the risk of cognitive impairment. Of the 6.8 million people in the U.S. that have some type of dementia, 5.4 million have Alzheimer’s disease today— projected to double by 2040.

More than 8 percent of all Americans have diabetes – either Type 1 (usually diagnosed in childhood requiring insulin injections) or Type 2 (typically involving weight gain in adulthood) – a number that is expected to grow with the rise in obesity. In diabetes, the body can’t produce enough insulin or use insulin properly to remove sugar from the bloodstream. When blood sugar remains too high, it can damage organs and lead to heart disease, kidney failure, nerve damage and other complications.

The relationship between diabetes and dementia drew new interest when a Japanese study – published in Neurology – that found that diabetics are twice as likely to develop Alzheimer’s disease. What’s more, even people with poor glucose control were 35 % more likely to develop some type of dementia.

According to published research, regular moderate exercise can reduce the risk of diabetes by half, and efforts to trim abdominal fat may reduce the rate of cognitive decline, since carrying significant belly fat raises the risk of late-onset Alzheimer’s disease in the middle-aged and elderly.

Posted in Alzheimer's Disease, epigenetics, How the Brain Works, How the Memory Works, Memory Fitness, Memory Health, neuroscience, Stroke, Uncategorized | View Comments

Brain Cell Epigenetics Plays Significant Role in Memory Fitness & Cognition

Researchers were surprised to discover that electrically stimulating activity caused massive amounts of dynamic changes to the epigenetic structure of neuronal brain cells that previously were thought to be highly stable.

As reported in Nature Neuroscience, results of recent mouse studies suggest major implications for treating neurodegenerative disorders such as Alzheimer’s disease, as well as psychiatric diseases, and for clearer understanding of the processes involved in learning, memory and mood regulation.

Specifically, researchers found evidence of an epigenetic change called demethylation—the loss of a methyl group from specific locations on the neurons’ DNA. Methyl groups, chemically referred to a CH4, turn on or off individual gene expression, thereby restricting the production of proteins prescribed by that gene. Therefore, when genes are turned off, their intended function is blocked. DNA makes up the fixed chemical building blocks of each genome. Adding or removing a methyl group, at a specific location, chemically affects DNA and the involved gene’s expression, enabling neurons with the same genetic code to perform differently.

In previously published work, these researchers reported that robust electrical brain stimulation resulted in enhanced neuroplasticity and increased brain cell growth in mice, due likely to changes in DNA methylation status. In the current mouse study, again using electric brain stimulation, the scientists analyzed 2 million neurons, focusing on one building block of DNA—cytosine—at 219,991 sites representing about 1 % of all cytosines in the whole mouse genomes.

After a few hours, scientists compared neurons in mice with or without brain stimulation. Thousands of sites – about 1.4 percent of the cytosines measured – showed rapid active demethylation or became newly methylated.

It now appears that epigenetic changes to neurons may be taking place all the time. This could explain how ‘identical twins’ don’t always get the same ‘inherited’ illnesses or why they may have totally different outcomes regarding dementia, stroke or other serious medical conditions.

In the future, safe and orderly controlled epigenetic regulation of gene expression may enable the reduction in diseases or conditions that impact maintenance of memory fitness and lowering the risk of Alzheimer’s disease, Parkenson’s and stroke.

Posted in Alzheimer's Disease, epigenetics, How the Brain Works, How the Memory Works, Memory Fitness, Neuroplasticity, Stroke, Uncategorized | View Comments

Help Maintain Memory Fitness With Another Cup Of Joe

The resurgence of coffee as health benefit is supported by accumulating research. Coffee holds a host of physical — not to mention psychological — benefits which scientists are now beginning to appreciate.
Scientific research suggests that roasted coffee – both caffeinated, decaffeinated and instant – contains over 1000 chemicals including more lipophilic antioxidants and chlorogenic acid lactones making it more protective against hydrogen peroxide-induced cell death in primary neuronal cells than green coffee. The espresso method of extraction yields higher antioxidant activity than other brewing methods. Antioxidants help reduce certain health risks, including cognitive decline.

Many people drink coffee for its ability to increase short term recall, according to a study reported in Science Daily. Frank Hu, MD, MPH, PhD, nutrition and epidemiology professor at the Harvard School of Public Health has reviewed many studies of coffee drinkers habits and their health status. While most studies are self reported – lacking conclusive medically valid proof – taken together, they certainly suggest more positives than negatives. For example, in cognitive tests of simple reaction time, choice reaction time, incidental verbal memory, and visuospatial reasoning, participants who regularly drank coffee were found to perform better on all tests, with a positive relationship between test scores and the amount of coffee regularly drunk. Elderly participants were found to have the largest effect associated with regular coffee drinking. Another study found that women over the age of 80 performed significantly better on cognitive tests if they had regularly drunk coffee over their lifetimes.

Coffee has also been linked to lower risk of dementia, including Alzheimer’s disease. A 2009 study from Finland and Sweden showed that, out of 1,400 people followed for about 20 years, those who reported drinking 3-5 cups of coffee daily were 65% less likely to develop dementia and Alzheimer’s disease, compared with nondrinkers or occasional coffee drinkers. Caffeine significantly decreases abnormal levels of the protein linked to Alzheimer’s disease.

Coffee may counter several risk factors for heart attack and stroke. First, there’s the potential effect on type 2 diabetes risk and heart rhythm disturbances, two risk factors for heart disease and stroke. Coffee has been linked to lower risks for strokes, especially in women, according to a study involving 83,700 nurses enrolled in the long-term Nurses’ Health Study. It showed a 20% lower risk of stroke in those who reported drinking two or more cups of coffee daily compared to women who drank less coffee or none at all. That pattern held regardless of whether the women had high blood pressure, high cholesterol levels, and type 2 diabetes.

Higher consumption of coffee is also associated with decreased risk of Parkinson’s and a reduced incidence of depression in women.

As usual, be sure to consult with your primary care provider to determine if and how much coffee is right for you.

Posted in Alzheimer's Disease, How the Brain Works, How the Memory Works, Memory Fitness, neuroscience, Stroke, Uncategorized | View Comments

Young Blood Promotes Growth Of New Brain Cells In Aging Brains

A decline in cognitive function – reduced attention skills, brain processing speed and reasoning ability – is a normal consequence of ageing. For some, the rate of this decline is accelerated and may go on to develop Alzheimer’s disease.

A recent study, published in Nature, shows that the blood of young mice contains proteins that can promote the generation of new brain cells in old mice. If substantiated, it may be possible to slow down or reverse this age-related decline in cognitive function.

Adult neurogenesis, a process in which neural stem cells continue to generate new cells throughout life, overturned the long-held view that the adult brain is incapable of regenerating itself and raised the possibility of developing stem cell-based therapies for neurological conditions such as dementia, stroke and Parkinson’s disease.
Neurogenesis occurs in two regions of the brain: the subventricular zone, generating cells that migrate to the olfactory bulb; and the subgranular zone, producing newborn cells that migrate into the hippocampus, critical for learning and memory formation. Normal age-related cognitive decline may be related to a reduction in the rate at which newborn cells are produced.

Because neural stem cells are located close to blood vessels, neurogenesis may be regulated by chemical cues in the blood. Experiments with mice twins found that pairs of young mice had about the same number of newborn neurons in the dentate gyrus as unpaired mice of the same age. This was also true for pairs of old mice. Remarkably, brains of old mice paired with young mice had many more new cells than unpaired old mice, and those of young mice paired with old ones had much fewer than unpaired young mice. In the adult brain, the only cells containing new DNA are those that have just been produced by the division of neural stem cells.

Chemicals found in the blood of old mice inhibit new brain cell generation, whereas chemicals in the blood of young mice promote it. Researchers then put blood from young or old mice into young adults. Again, they found that animals injected with old blood had far fewer newborn neurons in the hippocampus than those injected with young blood, confirming that old blood contains soluble factors that inhibit neurogenesis.

Investigating the effects of old blood on cell function, researchers took slices of hippocampal tissue from the brains of young mice paired with young and old ones, and using microelectrodes to examine electrical properties, a decrease in long-term potentiation (LTP) was observed. LTP, a form of synaptic plasticity, where connections between neurons are strengthened, is widely believed to be critical for learning and memory.

Speculating that changes in blood composition may be linked to age related cognitive decline, they trained young mice on two different tasks: a fear conditioning task; and a memory task. All of the mice performed similarly on both tasks. After the training, some mice were injected with blood from old mice, and made to perform the same tasks again. The performance of these animals on both tasks worsened.

Finally, researchers compared the proteins found in blood from young and old mice before and after pairing them with animals of the same or a different age. In young mice, the CCL11 protein decreased neurogenesis and impaired performance on the fear conditioning and memory tasks.

These results show that age-related changes in the composition of blood are linked to the decline in adult neurogenesis, suggesting that these rejuvenating factors have the potential to someday alleviate the age related decline in cognitive function.

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Statins May Protect Brain After Head Trauma And Stroke

A national study in the Journal of Trauma, suggests that statins may make traumatic brain injury much more survivable for older adults. Further, seniors on a statin at the time of moderate-to-severe head trauma were 76% less likely to die in hospital. The study reviewed outcomes through the National Study of Costs and Outcomes of Trauma database, which receives reports from 69 U.S. hospitals.

Statin users were also 13% more likely to have demonstrated a good functional recovery at 12 months following injury.

Although the effects of other cardiovascular factors seemed to negate any protective advantage, researchers suggested that statins should be further studied as possible protective agents to be immediately administered to patients with head trauma.

It should be noted that following damage from direct impact or acceleration and deceleration of the brain, secondary injury occurs from inflammatory and immune processes.

Researchers suspect that statins’ primary role in lowering cholesterol is unlikely to have any impact on brain injury patients’ recovery, but statins’ secondary effects on inflammation, thrombosis, and endothelial function may help prevent secondary injury. Animal studies have suggested a protective effect even when statins are started soon after brain injury.

While these researchers cautioned that this observational study could not imply a direct causal effect of statins, earlier research published in the journal Glia, found that statins – through experiments done in cell culture using human brain cells and exposing them to doses of statins used widely in patients – spur glial progenitor cells to develop into oligodendrocytes at a five fold rate versus normal levels. Glia – brain cells are known as ‘white matter’ – nourish and repair neurons (aka ‘grey matter’).

The body maintains a pool of uncommitted glial progenitor cells to turn to for ‘healing cells’ when it needs to repair damage from a variety of causes, such as an infection, hemorrhage, a serious blow to the head (TBI), or inflammation within the brain, such as in patients with multiple sclerosis or patients with stroke. Oligodendrocytes cells are ready to respond to any region of the brain that is damaged due to trauma, or lack of blood flow like a mini-stroke.

There really is nothing that can be prescribed to help people with a serious traumatic brain injury (TBI), recommendations are against administering statins for TBI until further confirmation of benefit and safety can be assessed. Additional research is needed in live humans to determine new interventions to patients with head trauma.

In the meantime, persons who take statins daily as prescribed by their doctor should consider its potential protective benefits in case of a stroke and a potentially key part of their life-span memory fitness plan.

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