Tag Archives: Alzheimer’s Disease

Scientists Develop Detection of Alzheimer’s Disease Blood Test

An international research team led by Hong Kong University of Science and Technology (HKUST) has developed a simple but robust blood test from Chinese patient data for early detection and screening of Alzheimer’s disease (AD) for the first time, with an accuracy level of over 96%.

Currently, doctors mainly rely on cognitive tests to diagnose a person with AD. Besides clinical assessment, brain imaging and lumbar puncture are the two most commonly used medical procedures to detect changes in the brain caused by AD. However, these methods are expensive, invasive, and frequently unavailable in many countries. 

The research team identified 19 plasma hub proteins (indicated as yellow dots in the figure) in AD patients, which are irregular compared to healthy people.

Now, a team led by Prof. Nancy IP, Vice-President for Research and Development at HKUST, has identified 19 out of the 429 plasma proteins associated with AD to form a biomarker panel representative of an “AD signature” in the blood.  Based on this panel, the team has developed a scoring system that distinguishes AD patients from healthy people with more than 96% accuracy. This system can also differentiate among the early, intermediate, and late stages of AD, and can be used to monitor the progression of the disease over time. These exciting findings have led to the development of a high-performance, blood-based test for AD, and may also pave the way to novel therapeutic treatments for the disease.

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Healthy choices may reduce Alzheimer’s risk

No effective treatment for Alzheimer’s disease exists, even though more than 5 million Americans have it, according to the Penn State Health News.

But what if there was a way to reduce the risk? Research suggests there may be methods to protect yourself.

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What is Alzheimer’s disease?

“Alzheimer’s is the most common form of dementia,” said Dr. Chen Zhao, a neurologist at Penn State Health Milton S. Hershey Medical Center. “With Alzheimer’s, an abnormal protein builds up in the brain, and over time, that spreads to other parts of the brain and normal brain cells start to die.”

This progression can lead to problems that affect one’s day-to-day life, including short-term memory loss, getting lost, spatial and navigation issues and trouble making judgments. It can eventually lead to trouble speaking or recognizing people.

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Protein Toxicity involved in Alzheimer’s triggered by a chemical ‘switch’

Researchers from Tokyo Metropolitan University have discovered that a specific chemical feature of a key protein known as tau may cause it to accumulate in the brain and trigger illnesses like Alzheimer’s. They found that disulfide bonds on certain amino acids act to stabilize tau and cause it to accumulate, an effect that got worse with increased oxidative stress. The identification of chemical targets triggering tau accumulation may lead to breakthrough treatments.

Tau proteins with cysteine groups bearing thiol groups (S) undergo chemical changes under oxidative stress to form disulfide bonds, making a toxic mutant of the tau protein that can aggregate. These go on to cause neural degeneration. Antioxidants can help reduce these back to thiols; these normal tau proteins can then be naturally cleared away by the cell. Illustration courtesy of Tokyo Metropolitan University

The tau protein is key to the healthy function of biological cells. It helps form and stabilize microtubules, the thin filaments that crisscross cell interiors to help keep them structurally rigid and provide ‘highways’ to shuttle molecules between organelles. However, when they are not formed correctly, they can accumulate and form sticky clumps. In the brain, these aggregates block the firing of neurons and cause a wide range of neurodegenerative diseases known as tauopathies, one of which is Alzheimer’s disease. It is vastly important that scientists find the ‘switch’ that transforms tau from an indispensable part of cell function to a deadly pathology.

A team led by Associate Professor Kanae Ando of Tokyo Metropolitan University has been using model organisms like the Drosophila fruit fly to uncover how specific features of the tau protein cause it to stop working properly. Flies can be genetically altered to express the same tau protein as in humans. By systematically modifying parts of the gene encoding for tau, they have been trying to pinpoint how certain features of mutant tau proteins affect their behavior.

In their most recent work, they found that alterations to amino acid residues in the protein known as cysteines in two different locations (C291 and C322) had a drastic effect on the amount and toxicity of tau. In a further breakthrough, the team pinned down the specific chemical feature responsible for making them toxic to normal cell function, that is, disulfide bonds formed by these cysteine groups. The toxic accumulation of tau got worse when cells were put in an environment with elevated levels of reactive oxygen species, as thiol groups on the cysteines were oxidized to form disulfide links. Biochemical environments with elevated oxidative stress are similar to those seen in patients with tauopathies. The co-expression of antioxidants to counter this effect helped natural processes clear away tau proteins, resulting in dramatically lower tau levels.

The team hope that knowledge of exactly which chemical groups are responsible for tau toxicity may lead to novel therapies which reduce or prevent tau accumulation, helping sufferers of tauopathies around the world.

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‘Rejuvenating’ the Alzheimer’s brain

Alzheimer’s disease is the main cause of dementia and current therapeutic strategies cannot prevent, slow down or cure the pathology. The disease is characterized by memory loss, caused by the degeneration and death of neuronal cells in several regions of the brain, including the hippocampus, which is where memories are initially formed. Researchers from the Netherlands Institute for Neuroscience (NIN) have identified a small molecule that can be used to rejuvenate the brain and counteract the memory loss.

New cells in old brains

The presence of adult-born cells in the hippocampus of old people was recently demonstrated in scientific studies. It suggests that, generally speaking, the so-called process of adult neurogenesis is sustained throughout adulthood. Adult neurogenesis is linked to several aspects of cognition and memory in both animal models and humans, and it was reported to sharply decrease in the brains of patients with Alzheimer’s disease. Researchers also found that higher levels of adult neurogenesis in these patients seem to correlate with better cognitive performance before death. “This could suggest that the adult-born neurons in our brain may contribute to a sort of cognitive reserve that could later on provide higher resilience to memory loss”, says Evgenia Salta, group leader at the NIN. Therefore, researchers from the NIN investigated if giving a boost to adult neurogenesis could help prevent or improve dementia in Alzheimer’s disease.

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Experimental drug shows potential against Alzheimer’s disease

Researchers have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them.

Researchers at Albert Einstein College of Medicine have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them. The study was published online today in the journal Cell.

“Discoveries in mice don’t always translate to humans, especially in Alzheimer’s disease,” said co-study leader Ana Maria Cuervo, M.D., Ph.D., the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases, professor of developmental and molecular biology, and co-director of the Institute for Aging Research at Einstein. “But we were encouraged to find in our study that the drop-off in cellular cleaning that contributes to Alzheimer’s in mice also occurs in people with the disease, suggesting that our drug may also work in humans.” In the 1990s, Dr. Cuervo discovered the existence of this cell-cleaning process, known as chaperone-mediated autophagy (CMA) and has published 200 papers on its role in health and disease.

CMA becomes less efficient as people age, increasing the risk that unwanted proteins will accumulate into insoluble clumps that damage cells. In fact, Alzheimer’s and all other neurodegenerative diseases are characterized by the presence of toxic protein aggregates in patients’ brains. The Cell paper reveals a dynamic interplay between CMA and Alzheimer’s disease, with loss of CMA in neurons contributing to Alzheimer’s and vice versa. The findings suggest that drugs for revving up CMA may offer hope for treating neurodegenerative diseases.

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How brain cells repair their DNA reveals ‘hot spots’ of aging and disease

Neurons lack the ability to replicate their DNA, so they’re constantly working to repair damage to their genome. Now, a new study by Salk scientists finds that these repairs are not random, but instead focus on protecting certain genetic “hot spots” that appear to play a critical role in neural identity and function, according to Science Daily.

The findings, published in the April 2, 2021, issue of Science, give novel insights into the genetic structures involved in aging and neuro-degeneration, and could point to the development of potential new therapies for diseases such Alzheimer’s, Parkinson’s and other age-related dementia disorders.

“This research shows for the first time that there are sections of genome that neurons prioritize when it comes to repair,” says Professor and Salk President Rusty Gage, the paper’s co-corresponding author. “We’re excited about the potential of these findings to change the way we view many age-related diseases of the nervous system and potentially explore DNA repair as a therapeutic approach.”

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Lifestyle often influential in Alzheimer’s patients – Study

For years, research to pin down the underlying cause of Alzheimer’s Disease has been focused on plaque found to be building up in the brain in AD patients. But treatments targeted at breaking down that buildup have been ineffective in restoring cognitive function, suggesting that the buildup may be a side effect of AD and not the cause itself.

A new study led by a team of Brigham Young University (BYU) researchers finds novel cellular-level support for an alternate theory that is growing in strength: Alzheimer’s could actually be a result of metabolic dysfunction in the brain. In other words, there is growing evidence that diet and lifestyle are at the heart of Alzheimer’s Disease.

“Alzheimer’s Disease is increasingly being referred to as insulin resistance of the brain or Type 3 Diabetes,” said senior study author Benjamin Bikman, a professor of physiology and developmental biology at BYU. “Our research shows there is likely a lifestyle origin to the disease, at least to some degree.”

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Dementia linked to increased pain years before diagnosis – HHS

People with dementia may experience increased levels of pain 16 years before their diagnosis, according to new research. The study, funded in part by NIA and published in Pain, is the first to examine the link between pain and dementia over an extended period.

Dementia and chronic pain both cause changes to the brain and can affect a person’s brain health. Although many people who have dementia also have chronic pain, it is unclear whether chronic pain causes or accelerates the onset of dementia, is a symptom of dementia, or is simply associated with dementia because both are caused by some other factor. The new study, led by researchers at Université de Paris, examined the timeline of the association between dementia and self-reported pain by analyzing data from a study that has been gathering data on participants for as many as 27 years.

The researchers used data from the Whitehall II study, a long-term study of health in British government employees. Participants were between the ages of 35 and 55 when they enrolled in the study. Using surveys conducted multiple times over the course of the study, the researchers measured two aspects of participant-reported pain: pain intensity, which is how much bodily pain a participant experiences, and pain interference, which is how much a participant’s pain affects his or her daily activities. They used electronic health records to determine whether (and when) participants were diagnosed with dementia.

Out of 9,046 participants, 567 developed dementia during the period of observation. People who were diagnosed with dementia reported slightly more pain as early as 16 years before their diagnosis, driven mostly by differences in pain interference. These participants reported steadily increasing pain levels relative to those who were never diagnosed with dementia. At the time of diagnosis, people with dementia reported significantly more pain than people without dementia.

The researchers note that, because the brain changes associated with dementia start decades before diagnosis, it is unlikely that pain causes or increases the risk of dementia. Instead, they suggest that chronic pain might be an early symptom of dementia or simply correlated with dementia. Future studies that include data on the cause, type, location, and characteristics of pain and the type and seriousness of a patient’s dementia could help define in more detail the link between dementia and pain.

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Exercise may help slow memory loss for people living with Alzheimer’s dementia – Study

Since my family has Alzheimer’s or dementia on both sides, this was one of those studies that resonated with me. Eat less; move more; live longer and think better.

Promising new research shows aerobic exercise may help slow memory loss for older adults living with Alzheimer’s dementia.

ASU Edson College of Nursing and Health Innovation Professor Fang Yu led a pilot randomized control trial that included 96 older adults living with mild to moderate Alzheimer’s dementia.

Participants were randomized to either a cycling (stationary bike) or stretching intervention for six months. Using the Alzheimer’s Disease Assessment Scale-Cognition (ADAS-Cog) to assess cognition, the results of the trial were substantial.

The six-month change in ADAS-Cog was 1.0±4.6 (cycling) and 0.1±4.1 (stretching), which were both significantly less than the expected 3.2±6.3-point increase observed naturally with disease progression.

“Our primary finding indicates that a six-month aerobic exercise intervention significantly reduced cognitive decline in comparison to the natural course of changes for Alzheimer’s dementia. However, we didn’t find a superior effect of aerobic exercise to stretching, which is likely due to the pilot nature of our trial. We don’t have the statistical power to detect between-group differences, there was substantial social interaction effect in the stretching group, and many stretching participants did aerobic exercise on their own.” Yu said.

The findings are described in a recently published article, Cognitive Effects of Aerobic Exercise in Alzheimer’s Disease: A Pilot Randomized Controlled Trial, in the Journal of Alzheimer’s Disease.

Yu says their results are encouraging and support the clinical relevance of promoting aerobic exercise in individuals with Alzheimer’s dementia to maintain cognition.

“Aerobic exercise has a low profile of adverse events in older adults with Alzheimer’s dementia as demonstrated by our trial,” said Yu. “Regardless of its effect on cognition, the current collective evidence on its benefits supports the use of aerobic exercise as an additional therapy for Alzheimer’s disease.”

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Exercise May Help Slow Memory Loss for People Living With Alzheimer’s Dementia

Exercise may reduce decline in global cognition in older adults with mild-to-moderate AD dementia. Aerobic exercise did not show superior cognitive effects to stretching in our pilot trial, possibly due to the lack of power. ASU Edson College of Nursing and Health Innovation Professor Fang Yu led a pilot randomized control trial that included 96 older adults living with mild to moderate Alzheimer’s dementia.

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Participants were randomized to either a cycling (stationary bike) or stretching intervention for six months. Using the Alzheimer’s Disease Assessment Scale-Cognition (ADAS-Cog) to assess cognition, the results of the trial were substantial.

The six-month change in ADAS-Cog was 1.0±4.6 (cycling) and 0.1±4.1 (stretching), which were both significantly less than the expected 3.2±6.3-point increase observed naturally with disease progression.

“Our primary finding indicates that a six-month aerobic exercise intervention significantly reduced cognitive decline in comparison to the natural course of changes for Alzheimer’s dementia. However, we didn’t find a superior effect of aerobic exercise to stretching, which is likely due to the pilot nature of our trial. We don’t have the statistical power to detect between-group differences, there was substantial social interaction effect in the stretching group, and many stretching participants did aerobic exercise on their own.” Yu said.

The findings are described in a recently published article, Cognitive Effects of Aerobic Exercise in Alzheimer’s Disease: A Pilot Randomized Controlled Trial, in the Journal of Alzheimer’s Disease.

Yu says their results are encouraging and support the clinical relevance of promoting aerobic exercise in individuals with Alzheimer’s dementia to maintain cognition.

“Aerobic exercise has a low profile of adverse events in older adults with Alzheimer’s dementia as demonstrated by our trial,” said Yu. “Regardless of its effect on cognition, the current collective evidence on its benefits supports the use of aerobic exercise as an additional therapy for Alzheimer’s disease.”

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Hearing and Vision Loss May Speed Development of Cognitive Problems

Cognitive decline ranges in severity from mild cognitive impairment (MCI) to Alzheimer’s disease and related dementias (ADRD). It is marked by memory loss and difficulty thinking and making decisions. Cognitive decline is a significant, common challenge to older adults’ well-being and their ability to live independently.

Today, cognitive impairment and ADRD are major global public health and social concerns as the population of older adults rises around the world. By 2050, more than 152 million people will be affected by these conditions. That’s why many countries, including the United States, see the prevention of ADRD as a key public health priority and are studying programs to help stem these diseases.

One way to prevent cognitive impairment and ADRD is to treat the problems that raise the risk for developing them. Two of these risk factors are hearing and vision loss. Currently, about 60 percent of people aged 70 years or older are affected by hearing loss, 40 percent are affected by vision loss, and 23 percent of older adults have both vision and hearing loss. Some studies have suggested that having both hearing and vision loss may be linked to poorer cognitive function or to a faster rate of cognitive decline.

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Apathy could predict onset of dementia years before other symptoms

Apathy – a lack of interest or motivation – could predict the onset of some forms of dementia many years before symptoms start, offering a ‘window of opportunity’ to treat the disease at an early stage, according to new research from a team of scientists led by Professor James Rowe at the University of Cambridge.

Frontotemporal dementia is a significant cause of dementia among younger people. It is often diagnosed between the ages of 45 and 65. It changes behavior, language and personality, leading to impulsivity, socially inappropriate behavior, and repetitive or compulsive behaviors.

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A common feature of frontotemporal dementia is apathy, with a loss of motivation, initiative and interest in things. It is not depression, or laziness, but it can be mistaken for them. Brain-scanning studies have shown that in people with frontotemporal dementia it is caused by shrinkage in special parts at the front of the brain – and the more severe the shrinkage, the worse the apathy. But, apathy can begin decades before other symptoms, and be a sign of problems to come.

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Physical exercise and dementia

Of all the lifestyle changes that have been studied, taking regular physical exercise appears to be one of the best things that you can do to reduce your risk of getting dementia according to the Alzheimer’s Society.

Several studies looking at the effect of aerobic exercise (exercise that increases your heart rate) in middle-aged or older adults have reported improvements in thinking and memory, and reduced rates of dementia.

Exercising in mid-life

Prospective studies follow the health and behavior of a group of people over time. Several prospective studies have looked at middle-aged people and the effects of physical exercise on their thinking and memory in later life. Combining the results of 11 studies shows that regular exercise can significantly reduce the risk of developing dementia by about 30 per cent. For Alzheimer’s disease specifically, the risk was reduced by 45 per cent.

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App predicts risk of developing Alzheimer’s

A new study from Lund University in Sweden shows that validated biomarkers can reveal an individual’s risk of developing Alzheimer’s disease. Using a model that combines the levels of two specific proteins in the blood of those with mild memory impairment, the researchers are able to predict the risk of developing Alzheimer’s. The researchers have also developed an app that doctors can use to give patients a risk assessment.

Oskar Hansson and his colleagues have been researching different biomarkers for a long time to produce better diagnostics at an early stage of Alzheimer’s disease. Over the past year, they have also developed accurate markers in blood tests for Alzheimer’s. The aim has been to identify the disease at an early stage of its progression, before the actual dementia stage, in order to begin treatment to ease symptoms, avoid unnecessary examinations and create a sense of security among patients.

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Is definition of Alzheimer’s disease changing? – Mayo Clinic

The National Institute on Aging and the Alzheimer’s Association are suggesting changes to the research definition of Alzheimer’s disease. There are new criteria to define what Alzheimer’s disease is and who has it — but only as it relates to clinical trials and research, and not the diagnosis in your doctor’s office, according to Jonathan Graff-Radford, M.D. of the Mayo Clinic.

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Previously, Alzheimer’s disease dementia was characterized by symptoms such as memory loss and changes in thinking and cognition. And that’s still the case when your doctor diagnoses Alzheimer’s disease dementia.

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Older people with early, asymptomatic Alzheimer’s at risk of falls

Falls are the leading cause of fatal injuries in older adults, causing more than 800,000 hospitalizations and about 30,000 deaths in the U.S. every year. Some risk factors are well-known — advanced age, problems with vision or balance, muscle weakness — but an under-recognized factor is early Alzheimer’s disease. Older people in the earliest stages of Alzheimer’s, before cognitive problems arise, are more likely to suffer a fall than people who are not on track to develop dementia.

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Researchers at Washington University School of Medicine in St. Louis have found that, in older people without cognitive problems who experience a fall, the process of neuro-degeneration that leads to Alzheimer’s dementia already may have begun. The findings, available online in the Journal of Alzheimer’s Disease, suggest that older people who have experienced falls should be screened for Alzheimer’s and that new strategies may be needed to reduce the risk of falling for people in the disease’s early stages.

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