Alzheimer’s brain plaques found in people with traumatic brain injury

A new study, published in the journal Neurology suggests people with traumatic brain injury (TBI) may have buildup of plaques similar to those found in the brains of Alzheimer’s patients. Although these amyloid plaques match, their spatial distribution differs.

A corresponding editorial says that over the past decade the rate of emergency department visits related to traumatic brain injury (TBI) has increased by 70% in the United States. The editorial also says an estimated three to five million Americans live with a TBI-related disability.

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TBI occurs when the brain experiences damage due to a sudden trauma.

Study author Prof. David Sharp, MD, of Imperial College London said:

"The study is small and the findings preliminary; however, we did find an increased buildup of amyloid plaques in people who had previously sustained a traumatic brain injury.”

"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved. People after a head injury aremore likely to develop dementia, but it isn't clear why. Our findings suggest TBI leads to the development of the plaques which are a well-known feature of Alzheimer's disease."

People who suffer from TBI can have a slew of medical issues. While some TBI patients may experience cognitive impairments or difficulty with sensory information, others might have display mental health issues such as anxiety or depression. Yet, another long-term risk factor TBI patients is dementia. Scientists do not know the exact mechanism behind this relationship, but recent studies have made some progress into understanding it.

Read more Slow walking speed may be a sign of Alzheimer’s onset, say scientists

For the study, researchers recruited 9 people with an average age of 44 who had a single moderate to severe TBI. Their brain injuries had occurred between 11 months and 17 years previously. The research team took an in-depth look at their brains by taking PET and MRI scans. The PET scans detected amyloid plaques in the brain and the MRI scans searched out evidence of cellular damage resulting from the trauma.

The scan results were compared with 10 people with Alzheimer's disease and nine healthy participants (control group).

Both the people with brain injuries and the people with Alzheimer's disease had plaques in the posterior cingulate cortex, which is affected early in Alzheimer's. The researchers also found that plaques were increased in patients with more damage to the brain's white matter.

Interestingly, the TBI group, but not the Alzheimer's group, also showed plaques in the cerebellum.

Prof. Sharp said:

"It suggests that plaques are triggered by a different mechanism after a traumatic brain injury."

"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved.

“It suggests that plaques are triggered by a different mechanism after a traumatic brain injury. The damage to the brain's white matter at the time of the injury may act as a trigger for plaque production."

The current study is a relatively small-scale trial, however, Prof. Sharp believes that if a substantial link can be found between brain injury and the onset of Alzheimer's disease, it might help neurologists uncover treatment and prevention strategies to reduce the progression of Alzheimer's at an earlier stage.

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Growth factor in brain may slow cognitive decline

A new study has found that older people with higher amounts of a key protein from the gene called brain-derived neurotrophic factor, or BDNF in their brains have slower decline in their memory and cognitive skills compared to people with lower amounts of protein from the gene.

People tend to experience decline in physical skills as they age. Although the physical decline is obvious, the brain also has a tendency to slow down.

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However, it is not certain that cognitive decline will occur in all older adults. When it does occur, the speed of decline may vary from person to person. Significant impairment can be seen in some individuals, while others may show virtually no change at all.

The reasons behind these neurological differences are mystery to scientists. Since ageing is a multifaceted process and the brain is a complex organ, clues to the causal factors of mental decline with age are difficult to connect.

Dr.Aron S. Buchman and colleagues at the Rush University Medical Center in Chicago, IL, aimed to explore the involvement of BDNF in age-based cognitive decline.

BDNF is a growth factor that encourages the growth of new neurons and synapses, and supports existing neurons. It can be found extensively in both the brain and the peripheral nervous system. Many studies have shown that it is crucial in various important operations, including the maintenance of long-term memories.
Much of the nervous system in mammals is arranged before birth, but parts of the brain retain the ability to grow new neurons in a process called neurogenesis. BDNF is one of the major participants in this creation of new brain substance.

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The role of BDNF in memory and the protection and development of neurons make it a key candidate for examinations into the cognitive decline seen in many ageing brains.

Rats born without the ability to create BDNF die soon after birth because of neural abnormalities. However, if BDNF is injected into the lateral ventricle of an adult rat, new neurons grow in the striatum, septum, thalamus and hypothalamus.

For the study, researchers recruited 535 people with an average age of 81. These participants were part of the Rush Memory and Aging Project and the Religious Orders Study. They were followed until death, for an average of six years. The participants took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and levels of the gene that codes for BDNF in the brain were measured.

The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared to the lowest 10%. The effect of plaques and tangles – 2 hallmarks of Alzheimer’s disease –reduced cognitive decline in people with high levels of BDNF. Cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.

The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3% and BDNF accounted for 2%.

Plaques and tangles can be found in the brains of people with Alzheimer’s. Scientists believe that the plaques and tangles negatively impact cognitive function. The study revealed that the effect of these markers on cognitive decline was reduced by 40% for individuals with the highest levels of BDNF.

Dr. Buchman said:
"This relationship was strongest among the people with the most signs of Alzheimer's disease pathology in their brains.

This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer's disease."

Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.

The study was published in the online issue of Neurology, the medical journal of the American Academy of Neurology.

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Gum disease may worsen Alzheimer’s symptoms

A new study published in the journal PLOS One suggests there is a link between gum disease and greater rates of cognitive decline in people with early stages of Alzheimer's disease.

Periodontitis or gum disease is an unpleasant condition, causing bad breath, bleeding and painful gums, ulcers and even tooth loss.

The disease is more common in women than men. Persistent bad breath and red, swollen or bleeding gums are common signs of the condition. Poor oral hygiene, smoking and diabetes are all risk factors for gum disease.

The disease is common in older people and may become more common in Alzheimer's disease because of a reduced ability to take care of oral hygiene as the disease progresses.

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Previous studies have shown that higher levels of antibodies to periodontal bacteria are associated with an increase in levels of inflammatory molecules elsewhere in the body. These inflammatory molecules have been linked to greater rates of cognitive decline in Alzheimer's disease.

For the latest study, first study author Dr. Mark Ide, from the Dental Institute at King's College London in the UK, and colleagues aimed to determine whether periodontitis or gum disease is associated with increased dementia severity and subsequent greater progression of cognitive decline in people with Alzheimer's disease.

The researchers gathered 59 participants withmild to moderate Alzheimer's disease. Their cognitive function was evaluated by taking cognitive tests and their blood sample was taken to measure inflammatory markers in their blood. The majority of participants (52) were followed-up at 6 months when all assessments were repeated.

The results showed that the presence of gum disease at study baseline was not related to participants' cognitive state at that point. However, it did appear to be associated to a six-fold increase in cognitive decline over a six-month follow-up period. Additionally, participants who had gum disease at study baseline showed an increase in blood levels of pro-inflammatory markers over the follow-up period.

Read more Anxiety may be an early indicator of Alzheimer's disease in older adults

The authors suggest that gum disease is associated with an increase in cognitive decline in Alzheimer's disease, possibly via mechanisms linked to the body's inflammatory response.

Dr. Ide said:

"A number of studies have shown that having few teeth, possibly as a consequence of earlier gum disease, is associated with a greater risk of developing dementia. We also believe, based on various research findings that the presence of teeth with active gum disease results in higher body-wide levels of the sorts of inflammatory molecules which have also been associated with an elevated risk of other outcomes such as cognitive decline or cardiovascular disease. Research has suggested that effective gum treatment can reduce the levels of these molecules closer to that seen in a healthy state."

Researchers admit that limitations of the study included the small number of participants. They advise that the link between gum disease and cognitive decline should be examined in a larger cohort. They said that the precise mechanisms behind this association are not fully clear and other factors might also play a part in the cognitive decline of participants.

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Prolonged stress destroys memory, new study reveals

According to a new study from researchers at The Ohio State University, long-term stress destroys memory, and the immune system plays a vital role in the cognitive decline.

Long-term stress has been known to cause chronic muscle tension, heart problems, and fertility problems in both men and women. Now, the latest study performed in mice and published in the Journal of Neuroscience suggests chronic stress causes inflammation in the brain, which ultimately leads to memory loss.

The researchers said that the study in mice could one day bring about treatment for repeated, long-term mental attack such as the ones sustained by soldiers, bullying victims, and those who have to deal with beastly bosses. [Read more Small heat shock proteins act as a model for Alzheimer’s treatment]

Lead researcher Jonathan Godbout, Associate Professor of neuroscience at Ohio State said:

"This is chronic stress. It's not just the stress of giving a talk or meeting someone new.”

The first of its kind study was aimed to build the link between short-term memory and prolonged stress. Researchers stressed out several mice by periodically putting a much more aggressive mouse into their cage. [Read more Eating sweet food forms memory of the meal – findings could encourage novel treatment for obesity]

After six days of exposure, the stressed mice could no longer recall the location of a hole to escape a maze, which they remembered easily before the stressful period began.

"The stressed mice didn't recall it. The mice that weren't stressed, they really remembered it," said Godbout.

The stressed-out rodents had changes in their brains, including inflammation brought on by their own immune system. Short-term memory loss was caused by inflammation in the brain, itself the result of the appearance of immune cells called macrophages.

Thus, the researchers pinned the brief memory loss on inflammation, and on the immune system. [Read more How many carbs should you eat if you’re trying to lose weight?]

Godbout said that the effect on memory and evidence that the inflammation in the brain is caused by the immune system are crucial new discoveries.

"It's possible we could identify targets that we can treat pharmacologically or behaviorally," he said.
John Sheridan, co-author and Associate Director of Ohio State's Institute for Behavioral Medicine Research believes it could be that there are ways to interrupt the inflammation.

The mice in the study were exposed to what psychologists call 'repeated social defeat' – in other words they were bullied by a dominant alpha mouse. This was aimed to mimic humans who experience chronic psychosocial stress. [প্রতিদিন কফি পান আপনাকে দীর্ঘদিন বেঁচে থাকতে সাহায্য করবে]

Researchers want to bring to light the secrets behind stress and mood and cognitive problems with a long-term goal of discovering ways to help people who are depressed, anxious and suffer from conditions such as post-traumatic stress disorder (PTSD).

They found that the bullied mice had problem with spatial memory and avoided social contact for up to four weeks, indicating depressive-type behavior.

The stress, it seemed, was causing the mice’s immune systems to attack their own brains, causing inflammation. [প্রতিদিন ফ্রেঞ্চ ফ্রাই খাওয়ার অভ্যাস আপনার মৃত্যু ত্বরান্বিত করতে পারে]

The researchers dosed the mice a drug known to reduce inflammation to see how they would respond. They found that neither the problem in their brain-cell nor the symptoms of depression went away. However, there were no more memory loss and inflammatory macrophages.

The finding led to the conclusion that post-stress memory problem is directly connected to inflammation, and the immune system, rather than brain damage. The impact on memory and confirmation that brain inflammation is caused by the immune system are important new discoveries, said Professor Godbout, and could open new avenues for immune-based treatments. [Read more Changes in brain occur 20 years before Alzheimer’s onset]

Sheridan concluded:

“Stress releases immune cells from the bone marrow and those cells can traffic to brain areas associated with neuronal activation in response to stress.”

“They're being called to the brain, to the center of memory.”

While this isn’t the first time researchers tried to find the link between chronic stress and memory loss, or between inflammation and depression, it gives a new, encouraging connection between all four. The doctors could be benefited by it which may enable them to prescribe more treatments for conditions that are focused on the immune system such as, depression, and anxiety.

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Saliva gland test may provide early detection of Parkinson’s disease

A study by researchers from the Mayo Clinic in Phoenix, Arizona, and Banner Sun Health Research Institute in Sun City, Arizona suggests saliva gland test could become a new way to test for early Parkinson's disease.

Parkinson’s disease is a progressive degenerative disorder of the central nervous system mainly affecting the motor system. It may gradually develop with a barely noticeable tremor in just one hand. But while a tremor may be the most well-known sign of Parkinson's disease, the disorder also commonly causes stiffness or slowing of movement. It also affects sleep, balance, blood pressure and smell.

The motor symptoms of Parkinson's disease result from the death of dopamine-generating cells in the brain. Death of brain cells occur primarily in an area of the brain called the substantia nigra, a region in the midbrain. There is no cure for Parkinson’s, but medications can help control symptoms, often dramatically. In some later cases, surgery may be advised. The disease mostly affects older people, although around 4% of cases are diagnosed before the age of 50 years. Men are in one and a half times higher risk for the disease than women. [Read more Cancer drug may protect against Alzheimer’s, say scientists]

According to Parkinson’s disease Foundation (PDF), a million Americans may be living with the disease, and around 60,000 new cases are diagnosed each year, while thousands remain undetected.

In 2009, an estimated 126,893 cases of Parkinson’s disease were reported in the UK.

Currently there is no test available to diagnose Parkinson’s disease accurately. Doctors usually check medical history, signs and symptoms, perform neurological examination etc. to diagnose the disease.

For the study, the researchers wanted to see if a procedure termed "transcutaneous submandibular gland biopsy" could provide an answer. The procedure extracts a core of gland tissue by inserting a needle into a salivary gland under the jaw. [Read more Top 5 Health Benefits of Omega-3 Fatty Acids]

They were looking for a protein in the cells that could indicate early Parkinson's disease. They took the biopsies from one salivary gland to test for it. In their earlier tests, the same biopsy could detect abnormal protein in 9 out of 12 patients with advanced Parkinson's.

They recruited 25 patients for the new test. These people had the disease for less than 5 years. They also recruited 10 healthy individuals as the control group. [Read more The power of music: It relieves pain during and after surgery]

Of the 25 patients, 19 had sufficient tissue for the study. The researchers tested the biopsied tissues to see if they contained the Parkinson's protein. The results were then compared with those of the healthy control group. [ওজন কমাতে প্রতিদিন আপনার কতটুকু কার্বোহাইড্রেট খাওয়া উচিৎ?]

The protein was found to be present in 14 out of 19 patients.

Study co-author Dr. Thomas Beach, PhD, a neuropathologist with Banner Sun Health Research Institute, said:

"This procedure will provide a much more accurate diagnosis of Parkinson's disease than what is now available. One of the greatest potential impacts of this finding is on clinical trials, as at the present time some patients entered into Parkinson's clinical trials do not necessarily have Parkinson's disease and this is a big impediment to testing new therapies."

Study author Dr. Charles Adler, PhD, neurologist and professor of neurology at the Mayo Clinic, said that using submandibular gland biopsies to test for early Parkinson's disease may help many people because, currently, testing after 10 years gives a far more reliable diagnosis than early testing.

The researchers hope that further studies will increase understanding of the disease and help develop better treatments. [Read more High levels of harmful chemical phthalates detected in people who eat fast food]

The study was published in the journal Movement Disorders.

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Blocking brain inflammation stops Alzheimer’s

Researchers from the University of Southampton have discovered that blocking the production of new immune cells in the brain can help prevent the progression of Alzheimer’s disease. Experts described the findings as “exciting” and said it could lead to new treatments for the disease.

Researchers said their discovery added weight to evidence that inflammation in the brain is what propels the disease. [Read more Drug slows Alzheimer’s by boosting brain’s ‘garbage disposal’ system]

Until now most drugs used to treat dementia have targeted amyloid plaques in the brain which are the hallmarks of Alzheimer's disease.

However, the new study, published in the journal Brain, suggests that progression of the disease could be halted by targeting inflammation in the brain, caused by a build-up of immune cells called microglia.

Alzheimer's is a progressive neurodegenerative disease that slowly destroys memory and cognitive skills, and eventually the ability to carry out the simplest tasks. It is the most common cause of dementia, accounting for about 60-70% of all dementia cases. Together with other forms of dementia, Alzheimer’s affects 47.5 million people worldwide. The disease gives rise to 7.7 million new cases each year.

Alzheimer’s has been recently ranked as the 6^th leading cause of death in the United States. An estimated 5.7 million Americans of all ages have Alzheimer’s, and by 2050 this number is projected to rise to closely 14 million.

Around 800,000 people in the UK are affected by the disease.

Age is one of the risk factors of Alzheimer’s. People over the age of 70 are at a higher risk of developing Alzheimer’s. [স্বল্প শর্করাযুক্ত খাদ্য তালিকায় আপনি কি খেতে পারেন?]

For their study, the researchers compared post-mortem brain tissue samples from healthy people with the brains of people of the same age with Alzheimer's disease. They found increased numbers of microglia in the tissue samples of people with Alzheimer's disease compared with the tissue samples of healthy people. Microglia is a type of cell that, among other things, helps regulate immune responses like inflammation. Previous studies have also suggested that these cells could play an important role.

Next, the scientists wanted to study microglia in mice. They found that mice that were given an oral dose of inhibitor to block a receptor - called CSF1R - responsible for the rise in microglia in their brains, had fewer memory and behavioral problems, compared with untreated mice.

The drug also prevented the loss of communication points between nerve cells in the brain which is commonly seen in people with Alzheimer's. [Read more Research shows narcolepsy medication modafinil will actually make you smart]

The scientists also discovered that the inhibitor did not reduce microglia levels below the number needed for healthy immune function, suggesting blocking CSF1R only eliminates excessive numbers of cells.

However, the treatment did not stop another well-known feature of Alzheimer's disease - build-up of toxic amyloid protein clumps in the animals’ brain.

"These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease," said Dr. Diego Gomez-Nicola, lead author and neuroscientist and researcher in biological sciences at Southampton.

Mark Dallas, a neuroscientist at Reading University, said the discovery could explain why drugs designed to treat Alzheimer’s have so far been unsuccessful. [Read more Is ghee healthier than butter?]

“Excitingly, it does however highlight new avenues for researchers to exploit and strengthens the case for targeting other cell types within the brain in the fight against Alzheimer’s,” he added.

For the next step, scientists are planning to build on these findings and work to find a safe drug to test in humans and see if blocking the action of CSF1R has the same effect.

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New research says circadian rhythm of genes in brain changes with aging

Researchers at the University of Pittsburgh School of Medicine discovered that a 24-hour circadian rhythm controls almost all brain and body processes, such as the sleep/wake cycle, metabolism, alertness and cognition.

According to Wikipedia, Circadian Rhythm is any biological process that displays an endogenous, entrainable oscillation of about 24 hours. These 24-hour rhythms are driven by a circadian clock, and they have been widely observed in plants, animals, fungi, and cyanobacteria.

The first-of-its-kind study, published in the journal Proceedings of the National Academy of Sciences, also suggest that a novel biological clock begins ticking only in the older brain.

"Studies have reported that older adults tend to perform complex cognitive tasks better in the morning and get worse through the day,"

"We know also that the circadian rhythm changes with aging, leading to awakening earlier in the morning, fewer hours of sleep and less robust body temperature rhythms.” said Colleen McClung, Ph.D., associate professor of psychiatry, Pitt School of Medicine.

Etienne Sibille, PhD, senior co-investigator and Campbell Family Chair in Clinical Neuroscience at the Centre for Addiction and Mental Health at the University of Toronto - had also previously shown that gene changes or "molecular aging" occurs in the brain.

Both teams set out to investigate the effects of normal aging on molecular rhythms in the human prefrontal cortex – part of the brain responsible for learning, memory and other aspects of cognitive performance. [ওজন কমাতে প্রতিদিন আপনার কতটুকু কার্বোহাইড্রেট খাওয়া উচিৎ?]

The researchers analyzed thousands of genes from brain samples of 146 people with no history of mental health or neurological problems whose families had donated their remains for medical research and for whom the time of death was known.

The brains were categorized depending on whether they had come from a person younger than 40 or older than 60. Next, they analyzed two tissue samples from the prefrontal cortex for rhythmic activity, or expression, of thousands of genes by using a newly developed statistical technique.

They used information about the time of death and identified 235 core genes that make up the molecular clock in this part of the brain.

The team discovered that the daily rhythm in all the classic “clock” genes were present in younger people. Older people however, seemed to have lost rhythm in many of these genes.

"As we expected, younger people had that daily rhythm in all the classic 'clock' genes," said Dr. McClung.

"But there was a loss of rhythm in many of these genes in older people, which might explain some of the alterations that occur in sleep, cognition and mood in later life."

The team was surprised to find a set of genes that gained rhythmicity in older individuals.

The findings could be helpful in developing treatments for cognitive impairment and sleep problems that may occur with aging, as well as a possible treatment for "sundowning," a condition which makes older people with dementia become agitated and confused in the evening.

Dr. Sibille explained the usefulness of the findings, saying:
"Since depression is associated with accelerated molecular aging, and with disruptions in daily routines, these results also may shed light on molecular changes occurring in adults with depression."

For further studies, the team is planning to explore the function of the brain's circadian-rhythm genes in lab and animal models. They also find out whether these circadian-rhythm genes altered in people with psychiatric or neurological illnesses,

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