Small heat shock proteins act as a model for Alzheimer’s treatment

New discovery by German scientists that small heat shock proteins can prevent uncontrolled clumping of proteins in the brain has opened a new frontier in developing drugs for Alzheimer’s treatment. The accumulation of beta amyloid plaques (abnormal clusters of chemically sticky protein fragments) between nerve cells in the brain is one of the hallmarks of Alzheimer’s disease.

Alzheimer’s disease is the most common form of dementia. It is fatal and progressive. The accumulation of amyloid plaques and neurofibrillary tangles are the prime suspects behind damage and death of nerve cells that destroy a person’s memory and cognitive skills.

There is no cure for Azlheimer’s but different drug and non-drug therapies can make a person live ably with the disease. [Read more 15 Reasons Why You Should Eat More Fish]

Alzheimer’s is the 6^th leading cause of death in the United States. An estimated 5.1 million Americans have Alzheimer’s.

In the UK, an estimated 850,000 people will have dementia by the end of 2015 and the number will rise to 1 million by 2025. Every year nearly 60,000 deaths are directly attributed to dementia.

Small heat shock proteins act as “helper” proteins and for the cells, they are the “catastrophe aid workers”. They play a wide range of roles, including guarding other proteins from becoming damaged. When vital cell proteins are exposed to intense heat or radiation, they lose their form and clot up, turning into entangled clumps. When the clumps are formed, these cells cannot be saved – they become useless and begin to die. That’s when the small heat shock proteins come to the rescue. 

They bind to the damaged proteins before they clod together helping them to restore their proper shape by preserving them in a soluble form. [Read more Scientists report significant breakthrough in anti-aging]

In Alzheimer’s disease, the small heat shock protein that stops the beta-amyloid from forming long fibrils and clog up cells in the brain is called alpha-B-crystallin.

The research team led by Bernd Reif, a chemistry professor at the Technical University of Munich (TUM) and a team from Helmholtz Zentrum München, shows exactly how alpha-B-crystallin collaborates with beta-amyloid to stop the formation of clumping in Alzheimer’s.

The researchers were able to identify the exact locations in the alpha-B-crystallin that bind to the beta-amyloid by using solid-state Nuclear Resonance (NMR) spectroscopy. [এসপারাগাসঃ স্বাস্থ্যগুণ, ভেষজগুণ এবং ইতিহাস]

"Alpha-B-crystallin exists in various different forms comprising 24, 28 or 32 subunits that are permanently being swapped. In addition, it has a large molecular weight. These factors make structure analysis very difficult,” Professor Reif explained the complexity of alpha-B-crystallin.

Prof. Reif and his colleagues – Johannes Buchner, and Sevil Weinkauf, both from TUM, found that these small heat shock protein utilizes a certain non-polar beta-sheet form mound in its center for communications with the beta-amyloid. This mechanism enables it to gain access to the aggregation process in 2 locations at once –

1.       It attaches to dissolved beta-amyoids, stopping them from formation of fibrils.

2.       It seals existing fibrils, therefore no more amyloids cannot accumulate.

For further study, the researchers want to closely examine the alpha-B-crystallin’s N-terminal region. As they discovered, it attaches to protein types that clump together in a disorderly fashion.

The research was published in the journal Nature Structural & Molecular Biology.

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Exposure to environmental toxin may increase risk of Alzheimer's

A study has found long-term exposure to environmental toxin beta-Methylamino-L-alanine (BMAA) produced by blue-green algal blooms may be associated with the development of beta-amyloid plaques and tau tangles – hallmarks of Alzheimer’s disease – in the brain.

Researchers have suspected a connection between environmental triggers and Alzheimer's disease since the discovery of an unknown illness that included features of dementia, Parkinson's disease and amyotrophic lateral sclerosis (ALS), which affected Chammoro villagers from the Pacific island of Guam in the 1960s. [Read more Can Turmeric Prevent Alzheimer’s?]

The toxin, BMAA is produced by cyanobacteria - a type of blue-green algae that are found in oceans, soil and lakes. The toxin is present in various marine lives, including sharks and shellfish, which ingest cyanobacteria and can also be found in plants, such as cycads.

The seeds of cycads are eaten by flying foxes, so BMAA is often present in these animals. Chamorro villagers use the seeds from this plant to make flour and also fish and flying foxes form a key component of their diet. Therefore, their diet is highly contaminated with BMAA.

The team led by Paul Alan Cox, PhD, an ethnobotanist at the Institute for EthnoMedicine in Provo, UT, had previously identified beta-amyloid plaques and tau tangles in the brains of Chamorro villagers who had died of paralytic illness. These villagers were exposed to high levels of dietary BMAA, as a result of consuming flying foxes.

The team, for the latest study, aimed to prove whether there is a link between dietary BMAA and development of neurodegenerative diseases. [Read more Art-making can reduce stress, even if you aren’t artistic]

To emulate the conditions experienced by the Chammoro villagers, Dr. Cox and his colleagues decided to expose the same toxin to vervet monkeys.

They conducted two experiments on the monkeys, in which they fed the animals various doses of dietary BMAA over 140 days.

The researchers conducted two experiments on vervet monkeys (Image: Creative commons)

The first experiment

The researchers divided the monkeys into 3 groups. The first group was fed fruit containing BMAA, the second group was fed fruit containing equal levels of BMAA and L-serine - a dietary amino acid – while the third group was fed fruit containing a placebo.

Upon analyzing the brain tissue of the monkeys, researchers found that those fed fruit containing only BMAA showed development of tau tangles and beta-amyloid plaques.

The group of monkeys who ate equal amounts of BMAA and L-serine, however, showed reduced tangles, while the group that were fed the placebo did not develop tangles and plaques at all.

Studies coauthor Deborah Mash, PhD, director of the University of Miami Brain Endowment Bank in Florida notes:

"The tangles and amyloid deposits produced were nearly identical to those found in the brain tissue of the Pacific Islanders who died from the Alzheimer's-like disease.”

Second experiment

The findings from the first experiment were replicated in the second experiment, in which the monkeys were divided into four groups. [Read more Changes in brain occur 20 years before Alzheimer’s onset]

The first group of monkeys was fed fruit containing BMAA at a dose similar to that consumed by Chamorro villagers. The second group ate fruit that contained a tenth of that dose. The third group received fruit containing equal amounts of BMAA and L-serine. The fourth group was given fruit containing placebo.

At the end of the 140 days, the researchers found all monkeys that consumed BMAA had developed tau tangles and beta-amyloid plaques.

Dr. Cox explained the results:

"Our findings show that chronic exposure to BMAA can trigger Alzheimer's-like brain tangles and amyloid deposits.”

“As far as we are aware, this is the first time researchers have been able to successfully produce brain tangles and amyloid deposits in an animal model through exposure to an environmental toxin."

Role of amino acid in preventing Alzheimer’s

As seen in the first experiment, monkeys that consumed an equal amount of L-serine alongside BMAA showed a significant reduction in tau tangles, suggesting the amino acid may hold promise for the treatment of Alzheimer's.

Dr Dunlop said the focus of research now was to investigate whether or not the amino L-serine that reduced the development of brain tangles in the experiment could help slow down the early stage of Alzheimer's disease in humans.

They also note that the US Food and Drug Administration (FDA) have not approved L-serine for the treatment of neurodegenerative conditions. [এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে]

But first, she said, scientists needed to work out if the supplement was safe. She cautioned:

"We cannot recommend that people start taking it."

"We are currently starting phase 1 trials in the US looking at the safety of this particular supplement in humans."

In the meantime, she said people could take simple steps to avoid exposure to the toxin.

"We're not suggesting people stop eating certain foods but ... if you're surfing or swimming or doing recreational activities in lakes that have green scum, it's probably not a good idea," she said.

Researchers however are working on the findings. The Institute for EthnoMedicine is conducting a phase 1 clinical trial alongside Dartmouth Medical School in Hanover, NH, in which they are evaluating the effects of L-serine among patients diagnosed with mild cognitive impairment (MCI) or Alzheimer's.

The study was published in the journal Proceedings of the Royal Society B.

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Bilingualism may protect against cognitive impairment from stroke

People who speak at least two languages are twice as likely as those who speak one language to have normal cognitive functions following a stroke, a new study finds.

Previous studies have shown that bilingualism may play a part in delaying the onset of Alzheimer’s disease.

"People tend to think of Alzheimer's as the only cause of dementia, but they need to know that stroke is also an important cause," said Subhash Kaul, D.M., senior investigator and developer of the stroke registry at Nizam's Institute of Medical Sciences (NIMS) in Hyderabad, India.

A stroke occurs when blood flow to a part of the brain is cut off. Burst of a blood vessel in the brain causes “hemorrhagic stroke,” and blocking of blood supply to the brain due to blood clot causes “ischemic stroke.” The cells in the brain are deprived of oxygen and glucose they need to survive, which causes the death of brain cells. If not detected early, stroke can cause permanent brain damage or even death. [Read more What Causes Aging? Can The Process Be Slowed?]

Stroke is a leading cause of disability in the US. Around 795,000 people have stroke each year, of them 185,000 are first time strokes. Stroke kills almost 130,000 Americans each year. On average, 1 person dies from stroke every 4 minutes in the US.

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 country.

In the new study, the researchers reviewed data of 608 stroke patients from Hyderabad, India, who were part of the NIMS stroke registry between 2006-2013.

More than half the patients were bilingual – defined by the researchers as speaking two or more languages. Other factors such smoking, high blood pressure, diabetes and age were also taken into account. [Read more Learning foreign languages may sharpen our minds]

The team found that 40% of bilingual patients had normal cognitive functions following a stroke, compared to about 20% of patients who spoke only one language.

Bilingual patients also produced better scores on post-stroke tests that measured attention and ability to retrieve and organize information.

The team was surprised to discover that there were no differences between bilinguals and single language patients in the likelihood of experiencing aphasia – a combination of a speech and language disorder caused by damage to the brain.

"The advantage of bilingualism is that it makes people switch from one language to another, so while they inhibit one language, they have to activate another to communicate," said Suvarna Alladi, D.M., lead author and a neurology professor at NIMS.

Moreover, Thomas Bak, M.D., study co-author at the University of Edinburgh in United Kingdom said: "The combined vocabulary of bilinguals can make it more difficult for them to find specific words. This may explain what appears to be a surprising result."

The results of the study may not be applicable to bilingual people all over the globe. In a multicultural city like Hyderabad, people commonly speak many languages such as, Telegu, Hindi, Urdu and English. [জেনে নিন গাজরের অসংখ্য না জানা গুণাবলী]

"Constantly switching languages is a daily reality for many residents of Hyderabad," explains Alladi.
"The cognitive benefit may not be seen in places where the need to function in two or more languages isn't as extensive."

According to Kaul, the findings do not necessarily suggest people who speak one language should begin learning another. He believes any mentally challenging task could be helpful.

"Our study suggests that intellectually stimulating activities pursued over time, from a young age or even starting in mid-life, can protect you from the damage brought on by a stroke," says Kaul.

The United States is largely monolingual. In fact, only about 15-20 percent of Americans consider themselves bilingual, compared to 56 percent of Europeans surveyed in 2006 by the European Commission.

The study was reported in the American Heart Association journal Stroke.

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Changes in brain occur 20 years before Alzheimer’s onset

Scientists have found that Alzheimer’s disease could be detected 20 years before the first symptoms appear. Finding could pave the way for early interventions to stop development of the disease.

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.

Read more: Awareness of memory problems may lessen 2 to 3 years before onset of memory loss or dementia

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.

Alzheimer’s has been recently ranked as the third leading cause of death in the United States. An estimated 5.3 million Americans have Alzheimer's, of whom 5.1 million are aged 65 and older.

Around 850,000 people in the UK are affected by the disease. [Read more High Levels Of Harmful Chemical Phthalates Detected In People Who Eat Fast Food]

It is a well-known fact that death of brain cells leads to the memory loss and behavioral changes that are associated with Alzheimer’s.

Scientists also know that brain cell death in Alzheimer's is related to a combination of inflammatory brain changes, described by German neuropathologist Alois Alzheimer as the 2 hallmarks of the disease. The 2 hallmarks are – 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 protein fragments called beta-amyloid. Scientists believe these plaques and tangles weaken communication between nerve cells, which in turn harms the processes that helps brain cells to survive.

However, scientists are not sure about exactly when plaques, tangles and inflammatory changes in the brain starts to take place – a fact that has been a mystery to the scientists all along. Now, principal researcher Professor Agneta Nordberg, of the Karolinska Institutet in Sweden, and colleagues believe their latest study has unraveled that mystery. [Read more Diabetes treatment may become ‘ouchless’ with the new insulin pill]

For the study, researchers scanned brains of more than 50 participants using positron emission tomography (PET). Some of these adults were at higher risk for Alzheimer's due to having relatives with gene mutations related to the disease, while some patients had non-inherited, "sporadic" Alzheimer's.

Prior to PET scans, all the participants were injected with 3 radioactive tracer molecules – PIB, Deprenyl and FDG. This enabled the researchers to track plaque levels and inflammation related to activation of astrocytes – the most common support cell in the brain.

In addition, glucose metabolism in participants’ brains was also measured, which provided insight into brain cell function. [এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে]

The researchers were able to identify plaques and inflammatory changes nearly 20 years prior to the estimated onset of memory problems among participants with Alzheimer’s-related gene mutations.

Researchers precisely found that astrocyte activation reaches its peak when plaques begin to accumulate in the brain.

Professor Nordberg explained:

“Inflammatory changes in the form of higher levels of brain astrocytes are thought to be a very early indicator of disease onset,”

“Astrocyte activation peaks roughly 20 years before the expected symptoms and then goes into decline, in contrast to the accumulation of amyloid plaques, which increases constantly over time until clinical symptoms show.”

“The accumulation of amyloid plaque and the increase in number of astrocytes therefore display opposing patterns along the timeline."

According to the researchers, brain cell function starts to decline approximately 7 years before the onset of Alzheimer’s disease symptoms.

Among people who did not possess Alzheimer's-related gene mutations, the team did not identify any such brain pathology. [Read more Scientists identify vital early warning of Alzheimer’s that could lead to improved treatment]

“Our research aims at understanding especially the earliest phases of the disease. Clinical trials aimed at clearing amyloid plaques have not yet succeeded at curing the disease, and therefore it is necessary to find new therapeutic targets,” said first author of the study Dr Elena Rodriguez-Vieitez.

The researchers believe that astrocytes could be a possible drug target for the condition. Reducing astrocyte activation early on could stop the disease from developing or change its course of progression.

The research was published in the journal Brain.

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Blood test for Alzheimer’s? New antibody test could accurately detect Alzheimer’s before symptoms appear

US researchers have developed an antibody test that can precisely detect if Alzheimer’s exist in a person before the symptoms appear. The test set to be available soon, will give physicians a chance to intercede at the earliest stage of the disease when treatment is possible.

Alzheimer’s disease is the most common form of dementia. It is fatal and progressive. The accumulation of amyloid plaques and neurofibrillary tangles are the prime suspects behind damage and death of nerve cells that destroy a person’s memory and cognitive skills.

The cause of Alzheimer’s is unknown and there is no cure for the disease, but different drug and non-drug therapies can make a person live ably with the disease.

Alzheimer’s is the 6th leading cause of death in the United States. An estimated 5.3 million Americans have Alzheimer’s. [Read more Mushrooms May Be Effective In Fighting Off Aging]

In the UK, an estimated 850,000 people will have dementia by the end of 2015 and the number will rise to 1 million by 2025. Every year nearly 60,000 deaths are directly attributed to dementia.

However, there is no definitive blood test for Alzheimer’s that has been approved by the FDA.

The research presented by Dr. Robert Nagele, PhD, at the American Osteopathic Association’s Osteopathic Medical Conference and Exposition (OMED15) in Orlando, Florida explains how antibodies act as blood-based biomarkers in order to detect countless diseases and identify the progression stage of the stage. [Read more Diabetes treatment may become ‘ouchless’ with the new insulin pill]

The researchers based their work on the hypothesis that thousands of autoantibody present in human blood specifically sticks to blood-borne cellular waste produced by organs and tissues in the body.  

A person’s gender, age and the presence of particular disease plays a role on his or her autoantibody profile. Attribute changes in autoantibody caused by diseases can perform as biomarkers that exhibit the presence of the disease. [Read more Anxiety may be an early indicator of Alzheimer's disease in older adults]

In Alzheimer’s, changes in the brain start to occur years before the symptoms appear. If the doctors are able to detect antibodies at the preclinical stage, it would give the patients a chance to work with the physicians to make lifestyle changes and receive treatments before symptoms appear. This process could eliminate or delay the most damaging symptoms.

While the cause of Alzheimer’s is unknown, researchers believe that a critical preventative measure can be taken by maintaining a healthy blood-brain barrier. [মধুর যত মধুর গুণাবলী]

Dr. Nagele points to the benefits of early detection of diseases because various conditions leading to vascular disease and risk factors for Alzheimer’s are similar. People who have preclinical disease can attempt to enhance their vascular health, such as controlling their diet, exercising and take steps to manage problems with blood pressure and weight in order to ward off slow progression of Alzheimer’s.

Other diseases such as Parkinson’s disease, multiple sclerosis (MS) and breast cancer could also be detected by this test. [Read more Eating alone may have dangerous effects on your health]

According to Jennifer Caudle, assistant professor of family medicine at Rowan University, physicians always endorse a healthy lifestyle to prevent diseases, but many people disregard the advice until a health crisis happens.

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Repeating words aloud to another boosts memory recall

You should read this if you are preparing for your exams, trying to memorize a speech or just trying to boost memory recall. A new study has found that repeating words aloud to another person can increase your verbal memory. Victor Boucher, a professor in the Department of Linguistics and Translation at University of Montreal said that the results of his study will be published in the next edition of the journal Consciousness and Cognition.

“We knew that repeating aloud was good for memory, but this is the first study to show that if it is done in a context of communication, the effect is greater in terms of information recall,” explained prof. Boucher. [Read more Eating fish weekly makes kids more intelligent and sleep better]

To demonstrate their findings on how to boost memory, Boucher and Alexis Lafleur, a doctoral student in neuropsychology asked 44 French-speaking university students to participate in a series of tasks.

For the first test, the participants were asked to read a number of lexemes from a computer screen. Lexemes are words written as they are found in the dictionary. During each stage of the test to boost memory, participants had to wear headphones that emitted “white noise.” This mechanism would mask their voices and thereby avoid auditory feedback.

For the next stage, participants were asked to repeat the words in 4 experimental conditions – repeat the words in their mind, repeat them silently by moving their lips, repeat the words aloud while staring at the screen and repeat the words aloud to another person. [Read more Learning foreign languages may sharpen our minds]

In the final stage of the test to boost memory recall, participants were made to engage in distraction task. After the completion of distraction task, they were shown another list of lexemes – some of which were shown to them before and some of which were not.

The results showed that performing the exercise aloud produced the highest verbal memory recall, while the least effective way to recall information was by repeating the lexemes in one’s head without gesturing.

According to Prof. Boucher, the simple way of communicating without making any sound generates a sensorimotor link that boosts our means to remember. But, we remember even more if the procedure is associated with the functionality of speech.

Another set of experiment was conducted in the test to boost memory recall. In this, the students were asked to repeat “non-words,” or chains of syllables that are not part of lexemes, in each of the four conditions mentioned before. [মধুর যত মধুর গুণাবলী]

The results showed that the students, repeating the non-words aloud to another did not show any higher verbal memory recall than repeating them in any of the other conditions. Boucher explains this as the brain’s inability to associate non-words with verbal memory. He noted that previous studies done by his team showed that the eloquence of a sound leaves a sensory and motor mark in the brain.

Boucher concluded by saying that a more coherent recall of the verbal element is created by the production of one or more sensory aspects. When talking to someone, aspects of sensorimotor and verbal expression are added to the brain’s multisensory information associated with the communication episode. Because of this, information is better retained in memory which shows that repeating words aloud to another person boosts memory recall.

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Alarming new study: Alzheimer’s disease may spread through blood transfusions

Can you catch Alzheimer’s? Can Alzheimer’s disease spread through blood transfusion? These questions have been asked by many, but there were no positive proof. But now, a new study suggests the disease might spread through blood transfusion.

Researchers from the University of British Columbia have found that healthy mouse who shared blood with another mouse who had Alzheimer's plaques did actually develop beta-amyloid plaques in its brain.

However, Professor Weihong Song, the lead researcher of the study said, people shouldn’t be frightened about catching Alzheimer’s disease through blood transfusions.

Read more Loneliness may be an early sign of Alzheimer’s disease, study finds

He said that in humans, beta-amyloid protein may pass through blood transfusions whether they have Alzheimer’s or not, because the protein can be manufactured outside the brain.

However, the chances of a healthy person developing beta-amyloid plaques in the brain via blood transfusion are very little because very low level of beta-amyloid can be exchanged. 

Beta-amyloid plaques are one of the hallmarks of Alzheimer’s disease. They are found between neurons in the brain. Beta-amyloid is a protein bit clipped from an APP (amyloid precursor protein). Inside the brain of a healthy person, these protein fragments get broken down and removed. However, in Alzheimer's patients, these sticky fragments gather to form solid, insoluble senile plaques.

Read more “Love hormone” Oxytocin may also enhance spiritual beliefs in men

Beta-amyloid protein starts to kill synapses – connections between neurons. After destroying synapses the protein clumps into senile plaque, which destroys the nerve cells.

The death of nerve cells cause the Alzheimer’s patient to gradually loose memory, learning and the person eventually becomes unfit to perform simple everyday tasks like tying shoelaces.

Alzheimer's cells showing beta-amyloid plaques

For their study, the team inserted beta-amyloid gene into healthy mice, which enabled the rodents to develop beta-amyloid plaques similar to the type seen in human Alzheimer’s patients.

The researchers then surgically attached each beta-amyloid gene carrying mouse to a mouse without the gene. The process simulated a shared blood system.

The healthy mice started to amass beta-amyloid in their brains, and after remaining attached for a year, the healthy mice developed Alzheimer’s. In the areas of the brain that were crucial for learning and memory, the infected mice showed destructive activities observed in Alzheimer’s.

Prof. Song said the protein can enter the brain from an attached mouse with beta-amyloid and cause neurodegeneration. [মধুর যত মধুর গুণাবলী]

A different study conducted last year, showed approximately 1.4 million who received blood transfusions from people with Parkinson’s disease and other forms of dementia in the UK, weren’t likely to get the diseases.

Professor Tara Spires-Jones of the University of Edinburgh, in the UK, said this is vital for us to understand the biological changes in our body and how toxic proteins spread, but this is very distant from Alzheimer’s disease in humans.

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

The phrase “Slow and steady wins the race” may not apply to all seniors. According to a research published in the journal Neurology, speed of walking in elderly people may indicate their probability of developing Alzheimer’s disease.

Slow walking is very common in elderly, but a research from France indicates it may be a sign of Alzheimer’s onset.

According to Dr. Laura Phipps of the Alzheimer’s Research UK, while Alzheimer’s disease is associated with forgetfulness and confusion, there may be other physical symptoms like mobility problems which may indicate Alzheimer’s.

Read more Art-making can reduce stress, even if you aren’t artistic

The research team led by Natalia del Campo, PhD, of the Gerontopole and the Center of Excellence in Neurodegeneration of Toulouse, in France, concluded that a slower pace of walking may be associated with the amount of beta amyloid Alzheimer’s patients have accumulated in their brains, even if the external symptoms of Alzheimer’s aren’t yet present in them.

The accumulated clumps of beta-amyloid are known as amyloid plaques. Amyloid plaques are considered one of the hallmarks of Alzheimer’s disease. Scientists believe build-up of amyloid plaques in and around hippocampus are responsible for the death of brain cells, which triggers the disease.

Alzheimer’s is the most common cause of dementia, accounting for about 60-70% of all dementia cases. The most common early symptom is short-term memory loss.

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

Read more What causes aging? Can the process be slowed?

Around 800,000 people in 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.

PET (Positron Emission Tomography) scans were performed on the participants' brains 

The team studied 128 seniors whose average age was 76 years, and were deemed at high risk of developing dementia because of their memory problems.

PET (Positron Emission Tomography) scans on their brains showed that 48% of them had amyloid levels often linked with dementia. Their cognitive skills and their ability to complete day-to-day activities were also tested.

Read more Awareness of memory problems may lessen 2 to 3 years before onset of memory loss or dementia

Of the participants, 46% had mild cognitive decline, which may indicate the start of dementia that arises in Alzheimer’s.

The participants’ walking speed was measured using a standard test that measures the time of how fast they walk approximately 13 feet at their own speed. The average walking speed of the seniors was 3.48 feet/second (2.3 miles/hour). All except 2 of the participants had normal walking speed.

The researcher discovered that amyloid levels accounted for up to 9 percent of the differentiation in the speed of walking. They found a connection between slow walking and amyloid in several parts of the brain, including putamen, a crucial area of the brain involved in motor function. The seniors who walked more slowly had greater accumulation of the protein amyloid. [এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে ]

There was no changes in connections between levels of amyloid and speed of walking, when their age, level of education or level of memory problems were taken into account.

Dr. del Campo says that it is possible that experiencing subtle walking disturbances along with memory concerns may indicate Alzheimer’s disease, even before any clinical symptoms are displayed. [Read more 7 Foods That Will Help You Lose Weight]

Del Campo notes, however, that the study only shows a link between amyloid and speed of walking but it does not prove that amyloid accumulation is the cause of slow walking. There are many factors that cause older people to walk slowly.

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Hearing loss tied to Alzheimer’s disease

As we get older, certain sounds become more difficult to hear. But, doctors say untreated hearing loss could put patients in risk for serious health problems.

“You can lose and additional cubic sonometer of brain tissue a year, if you have untreated hearing loss. That’s why it’s so important to test for it,” says neurologist Dr. Fredrick Shaerf in an interview with Lee Health.

According to experts, advanced hearing loss puts patients at risk for developing Alzheimer’s disease.

Read more Art-making can reduce stress, even if you aren’t artistic

Alzheimer's disease is a neurodegenerative disease that normally starts slowly and deteriorates over time. It is the most common cause of dementia, accounting for about 60-70% of all cases. While it starts out with short-term memory loss, the disease progresses rapidly, rendering the inflicted person unable to perform simple every tasks such as using the phone or tying shoelaces.

  

“There is significant risk of developing a dementia if they have untreated hearing loss; and those risks can be up to five times the risk if you have severe hearing loss, three times moderate, twice mild. So, that’s a significant risk with something that’s treatable,” Dr. Shaerf says.

Read more Lewy body dementia: Most misdiagnosed and often misunderstood

In 2016, the Better Hearing Institute highlighted the importance of hearing health to general cognitive function, due to a growing body of study linking untreated hearing loss to memory loss and decreased cognitive function.

Arthur Wingfield, PhD, Professor of Neuroscience at the Brandeis University, has been studying intellectual aging and the association between memory and hearing keenness for several years. He says that untreated hearing loss makes the person to put more effort while listening, which can lead to elevated stress and poorer results in memory tests.

Dr. Shaerf says that we don’t realize we have a hearing loss.

Hearing loss can be treated with things like hearing aids. About one-third of people who are 65 years or old, have hearing loss, but about 15 percent wear hearing aids.

“Well, it seems to be a risk because the information is not getting in. And therefore, in the speech and language centers, it’s not sort of not getting the stimulation, and we know when nerves don’t get stimulated, they shrink or atrophy,” Dr. Shaerf says.

Read more Brain electrodes may help Alzheimer’s patients keep memories

He recommends that patients have their hearing and cognition tests regularly.

“We also know that we don’t realize we have a hearing loss. And most of us who develop it lose some of the high-pitched tones so we hear the television when it’s up loud enough; we don’t think that there’s a problem, when there really is,” says Dr. Shaerf.

Recognizing and treating hearing loss early can prevent hearing loss problems, including the development of Alzheimer’s disease.

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Brain electrodes may help Alzheimer’s patients keep memories

Brain electrodes developed by researchers from the University of South Carolina and North Carolina’s Wake Forest Baptist Medical Center may help people suffering from memory loss and soldiers with brain-damage recapture their memories.

An estimated 5.5 million Americans have Alzheimer’s disease, according to a 2015 report. It is the sixth leading cause of death in the US. 1 in 3 seniors in the US die with Alzheimer’s or some other form of dementia. Alzheimer’s affects almost 800,000 people in the UK.

Read more Awareness of memory problems may lessen 2 to 3 years before onset of memory loss or dementia

In a normal brain, when sensory inputs in the forms of sights, sounds, smells, and feelings are sent, it creates a memory by sending complex electrical signals through the hippocampus region. 

Hippocampus is the part of the brain where memories are stored. The signals are then encoded at each region until it reaches the final region, where a completely different signal is sent for long-term storage.

However, if there is damage in any of the regions, it prevents the encoding and the brain fails to form a long-term memory. This is why Alzheimer’s patients can recall events that happened in the past before the brain damage, but cannot form new long-term memories due to hippocampus damage.

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

For the implant, electrodes are placed in hippocampus region of the brain. It has shown promising results in tests on rats and monkeys. Then they successfully used it on humans.

Researchers used patients with chronic seizures who had brain electrodes implanted in the hippocampus region of the brain for their treatment.

The brain electrodes were used on hundreds of trial that involved 9 patients, the algorithm accurately predicted how the signals would be translated about 90% of the time.

Ted Berger, a scientist from the Wake Forest involved with this project explains it like being capable of translating from Spanish to French without knowing either language.

This test suggests that a device can be designed to replace or support functions in the part of the brain that is damaged, said Robert Hampson of Wake Forest Baptist.

Researchers hope that this project with brain electrodes will help treat neurodegenerative disease like Alzheimer’s disease.

Brain electrodes are also being tested on paraplegics to help them perform simple movements with robotic arms or their limbs.

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Dr. Clare Walton, research manager at UK’s Alzheimer’s Society believes this device, if successfully tested in humans, could be an effective treatment for specific dementia symptoms, but it will not slow the progression of the disease or cure it.

Now, the researchers using brain electrodes are attempting to send back the translated signal in the brains of Alzheimer’s patients to try to bypass the damaged region, thereby allowing the formation of long-term memories.

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

A new study suggests anxiety may be an early warning sign of Alzheimer’s disease. The results support the theory that neuropsychiatric symptoms could depict the early signs of Alzheimer’s.

Researchers found that heightening symptoms of anxiety were associated with greater levels of beta-amyloid in the brains of elderly without impaired cognition. Beta-amyloid is a protein linked with Alzheimer's, and is one of the hallmarks of the disease.

Read more Urine test for early Alzheimer’s may be on the horizon

Scientists have long investigated risk factors, such as depression, that could result in Alzheimer’s. But this new study took a more distinct approach and examined the symptoms of depression – such as anxiety – itself.

Anxiety disorders, which affect almost 40 million adults each year, are common throughout the United States.

Alzheimer’s is a progressive neurodegenerative disease that causes cognitive decline and eventually renders the inflicted person incapable of carrying out simple tasks such as buttoning a shirt or using the phone. Approximately 5.5 million adults in the United States are affected by the disease, among them 5.4 million are older than 65 years.

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For their study, Dr. Nancy Donovan, from Brigham and Women's Hospital, and colleagues analyzed data of 270 healthy adults, who were part of the Harvard Aging Brain Study, for five years. The adults were aged between 62 and 90.

All the participants underwent positron emission tomography (PET) scan at the study onset and yearly during the 5-year follow-up period.

Researchers used 30-item Geriatric Depression Scale (GDS) to assess depression symptoms among these adults. They also evaluated scores for 3 conglomerations of depression symptoms: anxiety, apathy-anhedonia, and dysphoria.

Higher levels of beta-amyloid in the brain was linked with increasing symptoms of anxiety in older adults who didn’t have cognitive impairment.

The researchers found that higher levels of beta-amyloid in the brain was linked with increasing symptoms of anxiety in older adults who didn’t have cognitive impairment.

The findings suggest that increasing symptoms of anxious-depression may be an early sign of elevated levels of beta-amyloid, and in turn Alzheimer’s disease.

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The team says the results back the hypothesis that appearing neuropsychiatric symptoms constitute an early indication of preclinical Alzheimer’s.

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Dr. Donovan and her team concluded that a bigger study focusing on the same subject is required to further confirm these initial findings. However, the anxiety testing could be a practical tool to ascertain if a person is at heightened risk of developing Alzheimer’s disease, they added.

The findings were printed in The American Journal of Psychiatry.

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Urine test for early Alzheimer’s may be on the horizon

A joint study by Philadelphia’s Monell Chemical Sense Center and the U.S. Department of Agriculture (USDA) suggests the possibility of detecting early stages of Alzheimer’s disease from the odor signature of urine. Although the study was done on mice and a lot of work needs to be done, researchers are hopeful the findings will lead to a non-invasive urine test that diagnoses the neurodegenerative disease before it finds time to do too much damage to the brain.

Dr. Bruce Kimball, an author of the study, and a chemical ecologist with the USDA NWRC, said before this study they focused mostly on alterations in body smell caused by elements that derive outside the body, for example viruses and vaccines.

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Dr. Kimball said the findings may be useful for other neurologic diseases as well, since they now know that odor signatures of the urine can be changed by alterations in the brain typical of Alzheimer’s.

Alzheimer's is a progressive neurodegenerative disease that slowly destroys memory and cognitive skills, and eventually the ability to carry out simplest tasks. It is the most common form of dementia, accounting for about 60-70% of all dementia cases.

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

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

Although, the exact cause of the disease is not known, AlFuois Alzheimer, the German psychiatrist who described the disease, identified two hallmarks of the disease – abnormal quantities of protein (amyloid plaques) and fibers (tau tangles) in the brain.

While there is no way to reverse or stop the progression of this dreaded disease yet, an early and accurate diagnosis would provide patients and their caregivers time to plan and the healthcare professionals time to discover a treatment to ease the symptoms.

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For their study, the researchers worked with mice that artificially developed amyloid plaques in their brains same as the ones found in the brains of Alzheimer’s patients. For the breeding process, scientists inserted human genes into the genomes of the mice then used drugs to activate them. The mutations in the genes cause the brain cells of the mice to produce excessive amyloid precursor protein.

These types of mice are known as APP (amyloid precursor protein transgenic) mice. These mice similar behavioral symptoms of mental deterioration.

In the modified mice brain, the amyloid plaques clog the brain in a similar way that is observed in humans with Alzheimer’s disease.

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The researchers used three different strains of APP mice. After using behavioral and chemical analysis, the team discovered that each strain of these APP mice had specific urine smell signatures that were noticeably different from those mice in the control group.

The odor changes were not the result of new compounds being created in the body, but instead were changes in concentrations of normal urinary compounds.

The odor differences between control mice and those with Alzheimer's predated detectable quantities of plaque accumulation in the APP mice brains. Further studies revealed that the definite odor profiles could be used to pinpoint APP mice against control mice.

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Coauthor of the study Dr. Daniel Wesson, of Case Western Reserve University in Cleveland, said while this study is at the proof-of-concept stage, biomarkers to identify early-stage Alzheimer’s may someday be pinpointed by identifying distinctive odor signatures.

The findings were published in the journal Scientific Reports.

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