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.

Read more Exposureto environmental toxin may increase risk of Alzheimer's

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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Drug slows Alzheimer’s by boosting brain’s ‘garbage disposal’ system

A drug that increases activity in the brain’s "garbage disposal" system has been shown to reduce levels of toxic proteins associated with Alzheimer's disease and other neurodegenerative disorders and improve cognitive functions in mice.

The first of its kind research was conductedby neuroscientists at Columbia University Medical Center (CUMC) and published in the journal Nature Medicine.

Karen E.Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer'sDisease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute explained the findings:

"We have shown for the first time that it's possible to use a drug to activate this disposal system in neurons and effectively slow down disease.”

"This has the potential to open up new avenues of treatment for Alzheimer's and many other neurodegenerative diseases."

The drug used is known as rolipram. The drug is not considered safe to use in humans because it incurs side effect of nausea. However, other similar drugs do not cause nausea and could be used in clinical trials soon. [Read more Scientistsreport significant breakthrough in anti-aging]

Brain cells need to continuously clear out old, worn, or damaged proteins in order to stay healthy. A small molecular cylinder called proteasome does the clearing out job. It acts as a garbage disposal and grinds up the old proteins so they can be recycled into new ones.

In the brains of patients with neurodegenerative diseases, the proteasomes become damaged and they cannot do their job of clearing up. As a result, worn out proteins accumulate in the brain’s neurons. [ওজন কমাতে প্রতিদিন আপনার কতটুকু কার্বোহাইড্রেট খাওয়া উচিৎ?]

In Alzheimer’s disease, destruction and death of nerve cells causes the memory failure, personality changes and problems in carrying out daily activities.

The brains of people with AD have an abundance of two abnormal structures: 1) Amyloid plaques – consisting largely insoluble deposits of an apparently toxic protein peptide, or fragment, called beta-amyloid, and 2) Neurofibrillary tangles – abnormal collections of twisted protein threads whose main component is a protein called tau.

Scientists used a mousemodel of neurodegeneration and found that tau protein sticks to the proteasome and slows down the process of protein disposal.

When rolipram was administered in mice, it activated the proteasome and restored protein disposal to normal levels. The drug also improved the memory of diseased mice to levels seen in healthy mice. [Read more Bloodtest for Alzheimer’s? New antibody test could accurately detect Alzheimer’sbefore symptoms appear]

Past studies have shown rolipram’s effectiveness in improving memory in mice, but the mechanism wasn’t clear to scientists.

The new research pinpointed the mechanism, which showed that rolipram inhibits PDE-4 enzyme, thereby produces a a physical change in the proteasome that increases its activity.

The study’s first author, Natura Myeku, PhD, an associate research scientist in pathology and cell biology at CUMC tried to shed light on the mechanism:

"We still don't know exactly where the activation is happening, but what's new is that we can modify the proteasome to increase its activity. There could be many other ways to do this."

Researchers believe, drugs that work by targeting proteasomes should work for any disease caused by the accumulation of abnormal proteins, including Alzheimer's, Huntington's, Parkinson's and frontotemperoraldementia.

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Cancer drug may protect against Alzheimer’s, say scientists

Bexarotene – a drug approved in the US for the treatment of lymphoma – has shown potential in halting the first stages of Alzheimer’s disease, according to a research. Researchers are now looking at developing a treatment that can be taken as a preventative measure long before symptoms develop. However, they do not wish to propose bexarotene as a cure for Alzheimer's disease, but they suggest it could diminish the risk of developing the disease by boosting the body's natural defenses against faulty proteins in the brain.

German neuropathologist Alois Alzheimer described 2 hallmarks of Alzheimer’s disease – tau tangles developing inside neurons, caused by a build-up of tau protein, and amyloid plaques, developing between brain cells, caused by an accumulation of sticky protein fragments called amyloid beta. Scientists believe these plaques and tangles weaken communication between nerve cells, which in turn harms the processes that helps brain cells to survive.

Researchers found bexarotene after searching a library of 10,000 small molecules they assembled by looking for compounds that interact with amyloid beta. [Read more Exposure to environmental toxin may increase risk of Alzheimer's]

After observing the effects of these faulty proteins in a lab model of Alzheimer's, scientists have discovered that an already approved anti-cancer drug could delay the onset of the neurodegenerative disease. [Read more Eating sweet food forms memory of the meal – findings could encourage novel treatment for obesity]

Michele Vendruscolo, senior autho and a professor in the department of chemistry at the University of Cambridge said:

"By understanding how these natural defenses work, we might be able to support them by designing drugs that behave in similar ways."

For the study, Professor Vendruscolo and her colleagues – researchers from Cambridge, the University of Groningen in the Netherlands and Lund University in Sweden – worked with nematode worms that were engineered to develop Alzheimer's disease. At various stages of the disease, the worms were given the cancer drug, bexarotene, which has seen mixed results in treating Alzheimer’s in the past.

The researchers found that the drug disrupted the first steps in the process of amyloid plaque formation called primary nucleation. Primary nucleation occurs when naturally occurring proteins 'misfold' themselves and clump together with other proteins to form thin filament-like structures called amyloid fibrils, and smaller protein clusters called oligomers. However, the drug did nothing to combat symptoms that had already appeared, such as the appearance of dense clusters of beta-amyloid molecules. [Read more একা খাওয়া আপনার স্বাস্থ্যের জন্য মারাত্মক ক্ষতিকর হতে পারে]

"We showed that these worms that were doomed to develop Alzheimer’s disease could be rescued," said Prof. Vendruscolo.

Although research to prevent oligomer formation in Alzheimer’s has been going on for over 20 years, researchers have not made headway. Prof. Vendruscolo and colleagues believe this is because it is not known how the disease starts at the molecular level. [Read more Can Turmeric Prevent Alzheimer’s?]

Key finding of the study is that the researchers demonstrated exactly what happens at each stage of Alzheimer's disease, and what might be the result of a particular stage being interrupted or switched off.

This is not the first time bexarotene has been used in Alzheimer’s research. Earlier studies of bexarotene have suggested that the drug could actually reverse Alzheimer’s symptoms by clearing amyloid beta in the brain. The results however, were disputed. What this study has shown, is that the drug is ineffective in clearing protein clumps, but could play a role in stopping them from forming in the first place.

Co-author Prof. Chris Dobson said:
"Even if you have an effective molecule, if you target the wrong step in the process, you can actually make things worse by causing toxic protein assemblies to build up elsewhere."

Rosa Sancho, head of research at Alzheimer's Research UK, who was not involved in the study said:

"A recent clinical trial of bexarotene in people with Alzheimer’s was not successful, but this new work in worms suggests the drug may need to be given very early in the disease. We will now need to see whether this new preventative approach could halt the earliest biological events in Alzheimer’s and keep damage at bay in further animal and human studies."

The study was published in Science Advances.

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Breast cancer gene BRCA1 in the brain may be a factor in Alzheimer’s

American researchers have shown for the first time that low levels of BRCA1 protein in the brain may be a factor in Alzheimer's disease. BRCA1 is a key protein known for DNA repair. However, their mutated form increases the risk of breast and ovarian cancers.

The study published in Nature Communications and conducted by the researchers from the nonprofit Gladstone Institutes in San Francisco, CA, and the University of California-San Francisco (UCSF) illustrates that Alzheimer's is associated with a depletion of BRCA1 in neurons and that BRCA1 depletion can result in cognitive deficits. [Read more Eating sweet food forms memory of the meal – findings could encourage novel treatment for obesity]

"It's extremely interesting that one molecule can be critically involved in two apparently opposing conditions: cancer, in which too many cells are born and neurodegenerative disease, in which too many brain cells die off,” says senior author Lennart Mucke, a professor of neuroscience with roles in both organizations. [Read more Exposure to environmental toxin may increase risk of Alzheimer's]

When BRCA1 gene was discovered over 20 years ago, it was a breakthrough in cancer research. The discovery led to a blood test to identify inherited mutations linked to breast and ovarian cancers. Most recent estimate suggests that among women, who inherit a harmful BRCA1 mutation, 55 to 65 percent will develop breast cancer and 39 percent will develop ovarian cancer by the age of 70.

As mentioned earlier, BRCA1 plays an important role in DNA repair. Inside cells, DNA remains as a double helix containing 2 strands, like a twisted ladder. Repair protein BRCA1 fixes the strands if a break occurs once in a while. Broken strands that are not repaired normally trigger cell suicide.

Some scientists believe that defects in DNA repair may contribute to neurological disorders like Alzheimer’s. Alzheimer’s disease is known to cause death of brain cells. One of the hallmarks of the disease is build-up of beta amyloid proteins in and around brain cells. It is not clear whether the beta-amyloid proteins are responsible for the death of brain cells.

The researchers found reduced levels of BRCA1 protein, but not other DNA repair proteins, in post-mortem brains of Alzheimer's patients and also in the mice brains which were bred to develop a type of Alzheimer’s. [Read more What Is Celiac Disease And How Do You Treat It?]

When the BRCA1 gene in parts of the brains of healthy mice was knocked out, it expedited increased breaks in DNA and various neurological damages.

The scientists also experimentally reduced BRCA1 levels in the neurons of mice. The reduction of BRCA1 caused the mice to develop cognitive impairment.

The researchers were able to reduce the levels of BRCA1 by adding amyloid protein precursor molecules to brain cells growing in culture.

Increased DNA damage in brain cells that leads to dementia is the result of lower levels of BRCA1 protein caused by accumulation of faulty amyloid protein in the brain.

They are now testing whether increasing BRCA1 levels in mouse models can prevent or reverse brain damage and cognitive skills. [Read more একা খাওয়া আপনার স্বাস্থ্যের জন্য মারাত্মক ক্ষতিকর হতে পারে]

"The functions of BRCA1 in the brain remain to be fully elucidated, but our findings suggest that it may play an important role in supporting critical brain functions in both health and disease," concluded Professor Mucke.

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Experimental Alzheimer’s drug has anti-aging properties

A new study done by the researchers from Salk Institute in the United States has shown that an experimental drug aimed at fighting Alzheimer’s has the effect of slowing down aging in mice.

The study is the team’s embellishment of their past development of an experimental drug called J147, which works differently by targeting a major risk factor for Alzheimer’s – old age.

In their latest work, published in the journal Aging, the Salk researchers showed that this new drug candidate worked effectively in a mouse model of aging not generally used in Alzheimer’s disease studies. [Read more Scientists report significant breakthrough in anti-aging]

When the rodents were treated with J147, they showed improved memory and cognitive skills, while also displaying various enhancements in their psychological features and more robust blood vessels in the brain.

"Initially, the impetus was to test this drug in a novel animal model that was more similar to 99 percent of Alzheimer's cases," says Antonio Currais, the lead author and a member of Cellular Neurobiology Laboratory at Salk. [Read more What Causes Aging? Can The Process Be Slowed?]

"We did not predict we'd see this sort of anti-aging effect, but J147 made old mice look like they were young, based upon a number of physiological parameters."

Alzheimer’s is a chronic neurodegenerative disease. It is the most common cause of dementia. As mentioned earlier, age is one of the risk factors of Alzheimer’s and the disease starts slow but progresses with age. Plaques formed in the brain by beta-amyloid (pieces of protein) and neurofibrillary tangles causes the death of nerve cells in the brain.

People over the age of 70 are at a higher risk of developing Alzheimer’s. Approximately 80 percent of people over the age of 85 are affected by this dreaded disease.

Alzheimer’s has been recently ranked as the third leading cause of death in the United States. An estimated 5.3 million Americans of all ages have Alzheimer’s.

In UK, around 800,000 people are affected by the disease.

"While most drugs developed in the past 20 years target the amyloid plaque deposits in the brain (which are a hallmark of the disease), none have proven effective in the clinic," says David R. Schubert, a senior author of the study and a professor and laboratory head of Cellular Neurobiology Laboratory at Salk. [Read more 15 Reasons Why You Should Eat More Fish]

Several years ago, Professor Schubert and his team started to approach Alzheimer’s treatment from a new angle. Instead of targeting amyloid plaque, they decided to pinpoint the primary risk factor for the condition, which is old age. For this, they synthesized J147 by utilizing cell-based screens against brain toxicities that are caused by old-age.

In their previous study, the researchers discovered that J147 could stop and reverse Alzheimer’s pathology in mice with a version of the inherited type of Alzheimer’s. However, the inherited form is responsible for only about 1% of Alzheimer’s cases. For the rest, the prime risk factor is old age. Therefore, they set out to explore the drug’s effects on a breed of mice that age very fast and experience a type of dementia that is very similar to the age-related dementia in humans. [একা খাওয়া আপনার স্বাস্থ্যের জন্য মারাত্মক ক্ষতিকর হতে পারে]

The researchers, in their latest work studied 3 groups of rapidly ageing mice. They used an extensive set of trials to calculate the expression of all genes in the brain, and more than 500 small molecules responsible for the metabolism in the blood and brains of these mice. Of the three groups of rapidly ageing mice: one set was young, one was old and the other set was old but was fed J147 as they age. [Read more Slow walking speed may be a sign of Alzheimer’s onset, say scientists]

The group that was given J147 performed better on tests for memory and other cognitive skill and displayed stronger motor movements. The brains of these mice also showed fewer pathological signs of Alzheimer’s disease.

The scientists also noticed another remarkable effect – J147 prevented microvessels in the brains of these mice from leaking blood.

"Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.

The team believes that the only way to validate the clinical relevance of the study is to move J147 into human clinical trials for Alzheimer’s. They hope to start human trials next year.

Schubert said if it is proven safe, this anti-aging effect of J147 would help them in finding a way to slow aging.

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Antidepressants and Alzheimer’s drugs can also help stroke patients

Mounting evidence suggests that Alzheimer’s and antidepressant drugs may also help stroke patients recover.

A stroke can happen to anyone at any time. It occurs when a blood flow to an area of the brain is either blocked or severely reduced. When this happens, blood vessels cannot carry much needed oxygen and nutrients to that part of the brain. As a result, brain cells begin to die within minutes. Due to the death of brain cells, abilities controlled by that area of the brain such as memory and muscle control are lost. [Read more 15 Reasons Why You Should Eat More Fish]

There are 2 major types of strokes: Ischemic stroke – caused by a clot obstructing blood flow to the brain, and Hemorrhagic stroke – caused by ruptured blood vessel preventing blood flow to the brain. Another type of stroke, called “mini stroke,” is caused by a temporary clot.

A stroke in the right side of the brain will affect the left side of the body, leading to paralysis on the left side of the body and causing vision problems, speech problems, memory and other problems.

Stroke is the 5^th leading cause of death and the leading cause of disability in the United States. Each year, more than 795,000 people in the United States have a stroke which claims the lives of almost 130,000 Americans. One American dies from stroke every 4 minutes.

The good news is that strokes can be treated and prevented. Fewer Americans die of stroke today than 15 years ago. [Read more Scientists report significant breakthrough in anti-aging]

In the UK, around 152,000 people suffer a stroke each year. In 2010, stroke was ranked the fourth largest cause of death in the UK after cancer, heart disease and respiratory disease. The same year, stroke claimed the lives of 50,000 people in the UK.

About 1 in 3 stroke patients suffers from depression. This can lead to the patient’s inability to take part in rehabilitation.  

There is growing evidence that a class of antidepressants known as Selective Serotonin Reuptake Inhibitors (SSRIs) such as, Prozac, Paxil and Celexa, may also boost neurological recovery. Another type of antidepressant known as Norepinephrine Reuptake Inhibitor (NRI) also has shown to benefit neurological recovery.

The research team led by neurologists Dr. Xabier Beristain and Dr. Esteban Golombievski, of Loyola University Medical Center and Loyola University Chicago Stritch School of Medicine in Chicago, IL analysed 56 clinical trials of SSRIs. They found that the drugs seem to improve disability, dependence, neurological impairment, anxiety and depression after stroke.

There is also mounting evidence that a class of Alzheimer’s drug known as Acetylcholinesterase Inhibitors which includes, Aricept, Exelon and Razadyne, can improve aphasia in stroke patients.

Researchers are also studying a type of Alzheimer’s drug called Memantine (Namenda). When administered in combination with therapy, memantine showed language benefits lasting at least a year when compared with a placebo. However, clinical evidence of this drug for stroke recovery remains limited. [এসপারাগাসঃ স্বাস্থ্যগুণ, ভেষজগুণ এবং ইতিহাস]

There are some limitations to the study. Most studies conducted so far for stroke recovery have been small which employed different methods and time windows between stroke and clinical intervention.

"These medications have not yet been clearly proven to be of benefit to patients recovering from strokes," says Dr. Beristain.

Dr. Beristain and Dr. Golombievski concluded:
"We need well-designed, large clinical trials with enough power to establish the usefulness of medications as adjuvants to rehabilitation before we can routinely recommend the use of these agents to enhance neurological recovery after stroke."

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