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.

Showing posts with label News. Show all posts
Showing posts with label News. Show all posts

Saturday, January 26, 2019

Poor sleep increases Alzheimer’s brain proteins

poor sleep

A single night of poor sleep can cause a spike in brain proteins linked to Alzheimer’s disease, a new study reports.


Researchers from the U.S. and the Netherlands have found that sleep helps the body clear away two compounds in the brain, called amyloid and tau, and interrupted, poor sleep may cause too much of them to build up.

While the study doesn't show that poor sleep causes Alzheimer's, it adds one more piece to the puzzle of what causes dementia. [Read more Study:Access to nature makes men and seniors sleep better]
The team believes that the findings back the notion that chronic poor sleep in midlife could elevate the risk of developing Alzheimer's later in life.


“When people had their slow-wave sleep disrupted, their amyloid levels increased by about 10 percent,” says study leader Dr. Yo-El Ju of Washington University in St. Louis.

Although scientists knew there was a connection between dementia and poor sleep, it wasn’t clear whether dementia was driving insomnia or vice versa.

The study was jointly conductedby researchers from Washington University School of Medicine in St. Louis; Stanford University in California, in the U.S., and Radboud University Medical Centre in the Netherlands.

Alzheimer’s disease is a neurodegenerative disease that progresses rapidly. It is the most common cause of dementia, accounting for about 70% of all dementia cases. The disease affects memory, decision-making, language, thinking, and speech.

The brains of people with Alzheimer's disease feature two hallmarks of the disease – plaques of amyloid protein and tangles of tau protein. These plaques and tangles causes neuron cells to die.
In the UK, around 850,000 people are currently living with dementia, and the majority have Alzheimer’s disease, for which there is no cure. Although the number of dementia cases is dropping as people adopt healthier lifestyles, the number of people living with the illness is expected to rise to 1.2 million by 2040 because of the ageing population. [Read more Whatcauses aging? Can the process be slowed?]

More than a third of Britons also sleep for less than 6 hours a night, according to The Sleep Council.
For their study, the researchers sought to identify the most important phase of sleep.

“What we did was allow people to sleep a normal amount of time, but we prevented them from getting deep sleep or what is called slow-wave sleep,” Ju told NBC News.

“When we interrupted just the slow-wave sleep part, they still had an increase in amyloid. So this tells us it's getting the deep slow-wave sleep that's important for reducing the levels of amyloid.”
Ju and colleagues recruited 22 healthy adults aged between 35 and 65. All the participants reported experiencing no sleep problems and had no cognitive impairments.

The participants showed up in a controlled sleep lab. Half were allowed to sleep normally, while the other half were constantly kept in shallow sleep. [Read more Newprotein target may reverse memory loss in Alzheimer’s]

poor sleep

“As soon as they got into slow-wave sleep, they got a beep. And the beeps got louder and louder and louder until they came out of the deep sleep,” says Prof. Ju.

“It was pretty harsh.”

The participants didn’t realize their sleep had been interrupted, and this went on for the entire night.
The participants’ spinal fluid was analyzed in the morning.

“When people had their slow wave sleep disrupted, their amyloid levels increased by about 10 percent,” Prof. Ju says.

The subjects were also fitted with sleep monitors to measure theirsleep at home. Participants who experienced poor sleep at home were found to have higher levels of a second Alzheimer’s related protein called tau. [Read more Scientistsreport significant breakthrough in anti-aging]

Prof. Ju says they were not surprised to see that tau levels didn’t increase after only one night of poor sleep whereas this did cause amyloid levels to rise, since tau levels tend to change more slowly.
“But we could see, when the participants had several bad nights in a row at home that their tau levels had risen,” she adds.

Prof. Ju concludes by saying:

“At this point, we can't say whether improving sleep will reduce your risk of developing Alzheimer's. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer's disease. But a good night's sleep is something you want to be striving for anyway.”
Next, the team plans to study whether treating obstructive sleep apnea will improve people's slow-wave sleep and affect amyloid levels. Sleep apnea is a common cause of sleep disruption. People with this condition have a higher risk of developing dementia.

The study was published in the journal Brain.

Family History of Alzheimer’s May Explain Link of Metabolic Gene that Raises Risk for Disease

family history

Years of conflicting research that failed to pinpoint the missing link between a mitochondrial gene and the risk of Alzheimer’s may have finally been resolved by the scientists of Iowa State University (ISU) in the U.S. The researchers say that family history of Alzheimer's disease may be the missing link. It shows that having a family history of Alzheimer's disease appears to alter the behavior of the gene called TOMM40.

Lead researcher AurielWillette, assistant professor of food science and human nutrition at ISU, says the initial discovery of the gene TOMM40 gave the scientists impression that it raises the risk of Alzheimer’s. But the findings were later dismissed when several studies failed to replicate the results.
However, Willette and his colleagues weren’t convinced that the gene was a total failure, so they decided to examine other elements that may be producing the mixed results.

The researchers discovered a startling difference in the gene’s effect on cognitive function, memory and risk based on a family history of Alzheimer’s disease and the length of a specific part of the gene.
“It was kind of a shot in the dark, but we found if you don’t have a family history of Alzheimer’s disease, then having a longer version of the gene is a good thing. It is related to better memory up to 10 years later and about one-fifth of the risk for developing Alzheimer’s disease,” said Willette, who is also an adjunct assistant professor of neurology at the University of Iowa.

“However, if your mom or dad has Alzheimer’s, then having a long version is bad. It’s a complete polar opposite.”

The main pathological hallmarks ofAlzheimer’s disease are amyloid-β (Aβ) plaques, and neurofibrillary tangles, caused by tau protein. These plaques and tangles around the neurons eventually cause the neurons to die.

Outward symptoms start with mild memoryloss. As the symptoms progress, the person finds it increasingly difficult to hold a conversation or carry out everyday tasks such as button a shirt.
Although numerous studies being conducted worldwide are providing new clues, scientists still do not know the exact causesof Alzheimer's disease. They think that there are various factors, and some of these affect different people in different ways, according to the study.

family history of alzheimer's

Family history of Alzheimer’s and TOMM40

The researchers designed the study to explore the magnitude to which family history regulated the effects of TOMM40 on symptoms of Alzheimer's disease, such as thinking and memory loss.
They used data from two large studies of Alzheimer's disease. One set of data came from 912 adults in the Wisconsin Registry for Alzheimer's Prevention – a study which is following middle-aged adults at risk of developing Alzheimer's and following changes in cognitive function and memory loss, based on assessments carried out every 2 years for up to a decade.

The other set of data came from 365 participants in the Alzheimer's Disease Neuroimaging Initiative – a study which is monitoring similar changes in older adults with and without the disease.
The researchers found that having a family history of Alzheimer's disease appears to make a big difference in how TOMM40 affects memory and thinking, and that the difference depends on the length of a particular portion of the gene. [Read more Study:Access to nature makes men and seniors sleep better]

Prof. Willette and his team found that having the longer version of the gene, together with no family history of Alzheimer's, was linked to around a one-fifth lower risk of developing Alzheimer's disease and better memory up to 10 years later.

Family history was focused particularly on whether Alzheimer’s disease was found in a participant’s parents. The researchers also discovered a link between the family history, gene, and mitochondrial function, which produces energy to power the cells. Age, gender and education were controlled for in the examination of TOMM40 gene and family history in the participants.

The team is also involved in another project which is investigating factors that affect how the body makes and uses energy, such as insulin resistance, as well as proteins and enzymes that affect energy regulation.

Studies like these are slowly uncovering what happens to thinking and memory when there is not enough energy for brain cells to perform properly.

The study was published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.


Thursday, August 23, 2018

Alzheimer’s memory loss may be reversed by blocking a key enzyme


Alzheimers memory loss reversed by blocking HDAC2

Targeting an enzyme that interferes with memory-forming processes in Alzheimer’s patients can be an effective treatment for memory loss, according to a new study. A team of scientists from the Massachusetts Institute of Technology (MIT) in the U.S. found that it may be possible to reverse Alzheimer’s related memory loss with drugs that selectively impede the ability of the Histone deacetylase-2 (HDAC2) enzyme to interfere with the communication between brain cells.

Previously, scientists failed to target HDAC2because the drugs that were used also impeded other roles of the enzyme, causing toxic side effects.

The new research has shown that blocking a molecule called sp3 that binds to HDAC2 might effectively stop them both from disrupting the communication between brain cells that is crucial for memory.

"If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels," explains Seniorauthor Prof. Li-Huei Tsai, director of the Picower Institute for Learning and Memory at MIT, "then we can remove the blockade and restore expression of all these genes necessary for learning and memory."

For over a decade, Prof. Tsai has been researching the role that enzymes called HDACs play in memory loss. In2007, she discovered that blocking HDAC activity in mice could reverse memory loss. There are around a dozen types of HDAC in humans.

Alzheimer's disease is the most common form of dementia, affecting around 850,000 people in the UK. This neurodegenerative disease gradually diminishes a person’s ability to remember, think, reason, and make decisions.

There is no cure for thedisease and scientists do not know the causes of the disease. It is more common among people over 60 years, but it can affect younger people as well.
The new study focuses on the disruption of a process called synaptic plasticity, which is thought to be crucial for memory and learning.

Research has revealed that synapses – the connections between brain cells – are "plastic" and are not fixed as the soldered joints in electronic circuits.

Scientists define synaptic plasticity as a biological process whereby synapses change over time, depending on specific patterns of activity.


Scientists previously tested compounds that inhibit HDAC2, but most these produced side effects, such as interfering with HDAC1. HDAC1 is crucial for cell proliferation, especially in red and white blood cells.

Alzheimers memory loss reversed by blocking HDAC2


Therefore, in this new study, Prof. Tsai and his team sought to find a way to target only the HDAC2 activity that impedes memory. The team searched for proteins that help the enzyme to bind to the relevant genes.

To find the diabolical pairing, the researchers examined the expression of genes in postmortem brain samples taken from people who didn’t have Alzheimer’s.

Of these samples some brains had high and some had low levels of HDAC2, which helped the researchers to identify more than 2,000 genes that might be involved with HDAC2 activity.

Next, a technique called gene knockdown was used to prevent the expression of HDAC2 and other genes in mice. This narrowed down the search to a gene that made the protein Sp3.

Fragments of HDAC2 were used to connect with Sp3 in the mice. This effectively mopped up the proteins and prevented them from forming a complex with complete HDAC2 enzymes.

This clean-up was useful and it helped restore mice’s nerve functions, providing evidence that the enzyme and its helper were both required to latch onto the histones and DNA and prevent them from working.

The study was published in the journal Cell Reports.

Sunday, August 12, 2018

Oral health may be linked to cognitive decline


Oral health cognitive decline

According to new research published in the Journal of the American Geriatrics Society, there may be a link between oral health and the progression of cognitive decline.

"Clinical evidence suggests that the frequency of oral health problems increases significantly in cognitively impaired older people, particularly those with dementia,” said lead researcher Bei Wu, PhD, of Duke University's School of Nursing in Durham, North Carolina in the US.

"In addition, many of the factors associated with poor oral health — such as poor nutrition and systemic diseases like diabetes and cardiovascular disease — are also associated with poor cognitive function,” he added.

The researchers caution, however, that more studies are needed.

Findings came from the first systematic review of studies focused on oral health and cognition. These two important areas of research are important because in a growing older adult population, some 36% of people over age 70 are already living with some degree of cognitive decline. Researchers believe that a common inflammatory pathway may hold the key to a link between oral hygiene and cognitive impairment, if such a link exists.


Poor oral health has been blamed for heart disease, due to the spread of bacteria and oral health problems may be aggravated by diabetes and HIV/AIDS due to reduction of body’s resistance to infection.

Alzheimer's Association estimates around 5.4 million people in the US have Alzheimer's disease - the most common form of dementia.

To look for a link between oral health and cognitive status, Dr. Wu and her colleagues combed through 56 studies published between January1993 and March 2013 that examined the relationship between oral health and change in cognitive health or dementia incidence. They analyzed relevant cross-sectional (data collected at one specific point in time) and longitudinal (data collected over an extended period of time).

Some of the studies analyzed found that dental health measures, such as the number of teeth, the number of cavities, and the presence of gum disease, were linked to an increased risk of cognitive decline or dementia. Which is interesting considering a 2013 study found gum disease bacteria in the brains of Alzheimer’s disease patients — but this study in no way proved that gum disease causes Alzheimer’s disease. It just acknowledged an association.

However, researchers involved with the current review also noted that the findings based on the number of teeth or cavities are conflicting, and limited studies suggested that the dental conditions such as gingivitis are associated with cognitive decline. Similarly, the team didn’t regularly find that cognitive decline was associated with greater loss of teeth or number of decayed teeth. However, it is likely that "methodological limitations play a major role in explaining the inconsistent findings," they wrote.


"There is not enough evidence to date to conclude that a causal association exists between cognitive function and oral health. For future research, we recommend that investigators gather data from larger and more population representative samples, use standard cognitive assessments and oral health measures, and use more sophisticated data analyses," Dr. Wu said.

People with rosacea are at higher risk of Alzheimer’s


Rosacea linked to alzheimers

According to a new study people with rosacea – the facial redness affecting millions of people – are at an increased risk of developing dementia, particularly Alzheimer's disease, compared with people without the condition. The study also found that older patients and patients who were diagnosed by a hospital dermatologist were at the highest risk of developing Alzheimer’s.

However, the researchers were quick to point out that people with rosacea should not be overly concerned about the finding.

“It is important for patients to remember that having rosacea does not guarantee that they will develop Alzheimer’s disease,” said lead author Dr. Alexander Egeberg of the department of dermato-allergology at Herlev and Gentofte Hospital, in Copenhagen, Denmark.


“In fact, while the risk in rosacea patients may be slightly increased compared with the general population, the absolute risk [to any one patient] is still quite low,” he said.

Rosacea is very common, where some estimates suggest up to 1 in 10 people may have it. According to the National Rosacea Society, approximately 16 million Americans suffer from it. Around 1 in every 600 people in the UK are diagnosed with the condition each year. It most commonly affects people with fair skin, but can also occur in people of Asian and African origin. The condition is often mistaken for eczema, acne, or some other skin condition. Rosacea occurs in both men and women, but tends to be more common in women. Most cases are first diagnosed in people aged 30 to 50. There are no cures for the condition, but some medicines can alleviate symptoms.

The study was conducted by the team because there is evidence rosacea is linked with higher levels of certain proteins that have also been implicated in various neurological disorders, such as Alzheimer's disease and other forms of dementia. The proteins in question here are matrix metalloproteinases and antimicrobial peptides.

For the new study, Dr. Egeberg’s team analyzed data from the Danish nationalhealth registry system covering the period 1997-2012. The nation’s entire population – nearly 6 million men and women – were included, out of whom 83,500 had rosacea.

Individuals were followed until December 31, 2012, migration, a diagnosis of dementia, or death from any cause, whichever came first. Altogether, just over 99,000 developed dementia, including around 29,000 who were diagnosed with Alzheimer's disease.

After analysis, researchers found that people with rosacea had a 7% increased risk of dementia and a 25% increased risk of Alzheimer’s, compared with patients who did not have the skin condition. Older people were at higher risk.


The results also varied between men and women, where women with rosacea were at 28% increased risk of Alzheimer’s and men were at 16% increased risk.

For women, the raised risk of Alzheimer's linked to rosacea was 28 percent, whereas for men with the skin disorder it was 16 percent.

When the analysis was limited to cases of rosacea that had been diagnosed by a hospital dermatologist, the researchers found the increased risk of dementia was 42%, while the risk was 92% for Alzheimer’s disease.

Dr. Egeberg says:

"A subtype of patients have prominent neurological symptoms such as burning and stinging pain in the skin, migraines, and neuropsychiatric symptoms, suggesting a link between rosacea and neurological diseases."

"Indeed," he continues, "emerging evidence suggests that rosacea may be linked with neurological disorders including Parkinson's disease and now also Alzheimer's disease."

He says that the risk may be explained by certain underlying mechanisms shared by rosacea and Alzheimer's disease, but it is no known whether one causes the other.

The team suggests doctors should look out for symptoms of cognitive impairment in older patients with rosacea, and that only further studies can affirm if treating rosacea may also improve patients' risk of developing dementia.

The findings are published in the Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society.

Saturday, August 11, 2018

Belly Fat May Cause Cognitive Impairment


Belly fat cognition

A team of scientists from 3 Irish universities – St. James's Hospital and Trinity College Dublin, both in Northern Ireland, and Nutrition Innovation Centre for Food and Health at Ulster University – found that having higher levels of belly fat in old age is associated with a decrease in cognitive function.

Prevalence of Alzheimer’s and other forms of dementia is growing with the rise in average age of population. Currently, an estimated 47 million people worldwide are affected by dementia. This number is expected to rise to 75 million by 2030.

Scientists are trying to understand the risk factors involved in dementia as it will help us with potential interventions to lower the risk of this condition developing as we age. One such risk factor is obesity.

Earlier studies have shown that overweight or obese adults do not perform as well on tests of memory and visuospatial ability compared to those who are a normal weight. However, researchers aren’t sure if this trend continues into older age.

While previous studieshave looked into this matter, the results produced were contradictory. Since each study involved different forms of cognitive test, it is difficult to conduct a meta-analysis with the pooled results.

For this new study, the researchers set out to answer this question more conclusively using a large-scale trial. [Read more High-fat diet damages brain, affecting learning and memory]

The scientists from the three universities used data from the Trinity Ulster Department of Agriculture aging cohort study, which is a cross-border collaborative research project gathering data from thousands of adults over the age of 60 in Northern Ireland and Ireland.

Each of the 5,186 participants was assessed using a number of cognitive tests.

The team found that a higher waist to hip ratio was linked with reduced cognitive function. This could be due to an increased secretion of inflammatory markers by belly fat, which in previous studies had been linked with a higher risk of cognitive impairment.

On the contrary, bodymass index (BMI) measurements did not show the same trend; in fact, higher BMI was found to protect cognitive function. Researchers believe this is because BMI is a crude measure of body fat and cannot differentiate between fat and fat-free mass (muscle); it only takes into account weight and height.  

How cognition is influenced by belly fat?

Researchers believe that belly fat's impact on cognition might be due to high secretion of inflammatory markers – particularly C-reactive protein. This chemical is produced when fat cells send out signals. Increased levels of this have previously been linked to cognitive decline.

It should also be noted that according to studies, levels of inflammatory markers in the blood increases in the lead-in to dementia, before symptoms appear. 

Hemoglobin A1C (HbA1C) is another molecule that seemed crucial. When during their analysis, the researchers controlled for levels of HbA1C, the significant effect of belly fat on cognition disappeared.

The prevalence of obesity and dementia are putting enormous burdens on the society. Studies like this are crucial because by reducing obesity we may be able to curtail the prevalence of dementia.
The findings are published in the British Journal of Nutrition.

Sunday, July 15, 2018

New implantable capsule for Alzheimer’s prevention


implantable capsule for Alzheimer’s prevention
In a breakthrough Alzheimer’s treatment, scientists from the Ecole Polytechnique Federale de Lausanne (EPFL) in Switzerland have developed an implantable capsule that works by turning the patient's immune system against the disease. The lab of Patrick Aebischer at EPFL developed this bioactive capsule which contains cells that have been genetically engineered to produce antibodies against amyloid-β.

When German psychiatrist and pathologist Alois Alzheimer described Alzheimer’s disease for the first time in 1906, he brought to light the presence of two types of lesions in the brain – Senile plaques and Neurofibrillary tangles. Senile plaques are caused by over-accumulation of the protein Amyloid beta (amyloid-β) in different parts of the brain.

The capsule, when implanted under the skin, releases antibodies that travel to the brain and activate the patient's immune system to clear beta-amyloid protein.


Scientists have long been looking for ways to tackle these plaques, and they discovered one of the most promising ways to fight it is to “tag” the beta-amyloid proteins with antibodies that signal the immune system to attack and destroy them, before they can form plaques.

In the latest study, Mr. Aebischer of the Brain Mind Institute at EPFL and colleagues note that such a treatment needs to be administered in the early stages of memory loss in order to be most effective. The procedure requires repeat injections, which could have adverse effects.

They say their new implantable capsule could offer a safer and highly effectual alternative.

The capsule, described as a "macroencapsulation device," is made of two permeable membranes sealed together with a polypropylene frame. The device is 27 mm in length, 12 mm wide and 1.2 mm thick. It comprises cells taken from genetically engineered muscle tissue that can produce high levels of antibodies that are able to recognize and target beta-amyloid proteins in the brain.

The cells inside the capsule are made not only to be able to produce antibodies, but also to be compatible with patient, in order to not trigger the immune system against them, like a transplant can. This is where the capsule’s membranes come into play. The permeable membranes of the capsules allow the cells to soak up all the nutrients and molecules they need from surrounding tissue.

When the capsule is implantedin tissue under the skin, it gradually releases the antibodies into the bloodstream. The antibodies then travel from blood to the brain to track down and tag beta-amyloid
The device was successfully tested on mice which showed great success. The mice used were a genetic line of mice that is commonly used to replicate Alzheimer’s disease. The test showed substantial reduction of amyloid-β plaque load.

Verily, over a period of 39 weeks, the capsules produced a constant flow of antibodies, which prevented the formation of amyloid-β plaques in the brain. The treatment also decreased the amount of phosphorylation of the protein tau seen in mice. Tau protein is also believed to play a role in Alzheimer's development by forming "tangles" – another hallmark of the disease.

The proof-of-concept study has been hailed as a landmark. The researchers say it clearly demonstrated that implantable capsules can be used safely and successfully to deliver antibodies in treating Alzheimer’s and other neurodegenerative diseases that feature defective proteins.

Exercise may protect against cognitive decline


Exercise may protect against cognitive decline

A new study conducted by researchers at the University of Miami in Florida, suggests exercise in older age may slow the rate of cognitive decline and knock off a decade of the brain.

Researchers found that adults over the age of 50 who engaged in light or no exercise showed a significantly faster decline in memory and cognitive skills, compared with those who engaged in moderate to intense exercise.

Similar research in the past suggested that any amount of exercise may reduce the risk of Alzheimer's disease by 50%.

Although, these types of studies are in abundance, researchers say it is important to understand how cognitive decline may be slowed by lifestyle factors, especially with an ageing population.

Dr.Clinton B. Wright, of the University of Miami in Florida notes:

"The number of people over the age of 65 in the United States is on the rise, meaning the public health burden of thinking and memory problems will likely grow.”

"Our study showed that for older people, getting regular exercise may be protective, helping them keep their cognitive abilities longer."

For the study, the researchers evaluated data of 876 adults aged 50 and older - an average age of 71 - free of memory and thinking problems that were part of the Northern Manhattan Study.
Participants were asked how often they had exercised in the previous 2 weeks and how long they had exercised for.


Almost 90% of the participants said they engaged in either light exercise or no exercise at all. The other 10% reported engaging in moderate to high-intensity exercise, such as running, aerobics or calisthenics.

Approximately seven years later, participants had to take part in memory and thinking tests and undergo brain imaging with Magnetic Resonance Imaging (MRI). The same cognitive tests were completed again five years later.

Participants who engaged in light or no exercise demonstrated a decline in memory and thinking skills compared with participants who did moderate or high-intensity exercise over a 5-year period. Researchers said the difference was comparable to 10 years of ageing.

According to the research team, this association remained after accounting for a number of potentially confounding factors, including alcohol consumption, smoking, body mass index (BMI) and blood pressure.

Dr. Wright said:

"Physical activity is an attractive option to reduce the burden of cognitive impairment in public health because it is low cost and doesn't interfere with medications.

Our results suggest that moderate to intense exercise may help older people delay aging of the brain, but more research from randomized clinical trials comparing exercise programs to more sedentary activity is needed to confirm these results."

The study was published online in the journal Neurology.

Saturday, June 23, 2018

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


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

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

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


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

Study author Prof. David Sharp, MD, of Imperial College London said:
"The study is small and the findings preliminary; however, we did find an increased buildup of amyloid plaques in people who had previously sustained a traumatic brain injury.”

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

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


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

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

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

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

"It suggests that plaques are triggered by a different mechanism after a traumatic brain injury."
"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved.
“It suggests that plaques are triggered by a different mechanism after a traumatic brain injury. The damage to the brain's white matter at the time of the injury may act as a trigger for plaque production."

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

Growth factor in brain may slow cognitive decline


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

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

Read more Blocking brain inflammation stops Alzheimer’s


Growth factor in brain may slow cognitive decline

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

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

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

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

Read more Scientists identify vital early warning of Alzheimer’s that could lead to improved treatment

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

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

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

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

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

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

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

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

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

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

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


Monday, May 7, 2018

Prolonged stress destroys memory, new study reveals


stress destroying memory

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.

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


Saliva gland test

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.