What is Alzheimer's Disease?

Scientists aren’t absolutely sure what causes cell death and tissue loss in the Alzheimer's brain, but the plaques and tangles are prime suspects.

Does Memory Loss Always Mean Dementia?

Dementia is a broad category of symptoms that affect the brain and causes memory loss.

Early onset Alzheimer's

Although, Alzheimer’s is viewed as a disease of the elderly, up to 5% of Americans with Alzheimer’s have the early-onset variety, which can start to show symptoms as early as one’s 30s.

Saturday, February 17, 2018

Cancer drug may protect against Alzheimer’s, say scientists


cancer drug

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.

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


brca1 gene

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.

Tuesday, February 13, 2018

Experimental Alzheimer’s drug has anti-aging properties


experimental drug

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.

Monday, February 12, 2018

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 5th 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."

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


small heat shock proteins

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 6th 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.

Tuesday, February 6, 2018

Exposure to environmental toxin may increase risk of Alzheimer's

environmental toxin

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.

environmental toxin
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.

Bilingualism may protect against cognitive impairment from stroke

bilingualism

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.

bilingualism

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.

Sunday, February 4, 2018

Changes in brain occur 20 years before Alzheimer’s onset

Changes in brain occur 20 years before Alzheimers

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.


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.

Saturday, February 3, 2018

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

Blood test for Alzheimer’s

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.

Friday, February 2, 2018

Repeating words aloud to another boosts memory recall

repeating words aloud

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]

repeating words aloud

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.