Can exercise slow down Alzheimer’s?

A proof-of-concept brain imaging study suggests that exercising four or five times a week may delay the progression of Alzheimer’s disease in people who already have toxic buildups of beta-amyloid protein.

The new research is a 1-year randomized controlled trial led by Prof. Rong Zhang. The team published their findings in the Journal of Alzheimer’s Disease.

Prof. Zhang is affiliated with the departments of neurology, neurotherapeutics, and internal medicine at the University of Texas Southwestern Medical Center, in Dallas.

Full story at Medical News Today

The seeds of parkinson’s disease: Amyloid fibrils that move through brain

Researchers in Japan have found that the structure of Parkinson’s disease-associated protein aggregates can tell us, for the first time, about their movement through the brain. These new findings indicate that Parkinson’s disease is a kind of amyloidosis, which has implications for its diagnosis and treatment.

Lewy bodies, primarily composed of α-synuclein proteins (α-syn), are the neuropathological hallmark of Parkinson’s disease. However, we don’t yet fully understand how or why they appear in the brain. Using state-of-the-art imaging techniques, researchers at Osaka University have found that Lewy bodies in Parkinson’s disease brains contain α-syn protein aggregates (called amyloid fibrils) that can propagate through the brain. These findings, published this week in PNAS, support the new idea that Parkinson’s disease is a kind of amyloidosis, which is a group of rare diseases caused by abnormal protein accumulation.

“Our work follows on from in vitro findings that aggregates of α-synuclein that can propagate through the brain have a cross-β structure,” says lead author of the study Dr Hideki Mochizuki. “Our study is the first to find that aggregates in Parkinson’s disease brains also have this cross-β structure. This could mean that Parkinson’s disease is a kind of amyloidosis that features the accumulation of amyloid fibrils of α-synuclein.”

Full story at Science Daily

How chikungunya virus may cause chronic joint pain

A new method for permanently marking cells infected with chikungunya virus could reveal how the virus continues to cause joint pain for months to years after the initial infection, according to a study published August 29 in the open-access journal PLOS Pathogens by Deborah Lenschow of Washington University School of Medicine in St. Louis, and colleagues. According to the authors, uncovering the mechanisms for long-term disease could aid in the development of treatments and preventative measures for this incapacitating, virally induced chronic arthritis.

Chikungunya virus is spread by mosquitoes and causes severe joint and muscle pain. Approximately 30 to 60 percent of people infected with the virus continue to experience joint pain for months to years after the initial infection. However, the cause of this persistent joint pain is unclear, as replicating virus cannot be detected during the chronic phase. To address this question, Lenschow and colleagues developed a reporter system to permanently mark cells infected by chikungunya virus.

Using this system, they show in mice that marked cells surviving chikungunya virus infection are a mixture of muscle and skin cells that are present for at least 112 days after initial virus inoculation. Treatment of mice with an antibody that blocks chikungunya virus infection reduces the number of marked cells in the muscle and skin. Moreover, surviving marked cells contain most of the persistent chikungunya virus RNA. Taken together, the findings provide further evidence for musculoskeletal cells as targets of chikungunya virus infection in the acute and chronic stages of disease. According to the authors, this reporter system represents a useful tool for identifying and isolating cells that harbor chronic viral RNA in order to study the mechanisms underlying chronic disease.

Full story at Science Daily

Dementia Care in Assisted Living Homes

ALZHEIMER’S DISEASE AND dementia are becoming an increasingly big part of the health care conversation in America as the population ages and more people develop these cognitive ailments. The Centers for Disease Control and Prevention reports that about 5 million people are living with Alzheimer’s disease today, a figure that’s anticipated to nearly triple to 14 million by 2060.

For many people, once dementia has progressed to a certain level, they may need more care than family members can provide and may need to be placed in a long-term care facility– either an assisted living community or a nursing home.

Some of these facilities provide amazing care and support of older adults dealing with cognitive decline or dementia. Others may not. And if you’re considering placing a loved one into an assisted living facility that offers dementia care, there are a few factors you should consider when evaluating whether a specific community is the right one.

Full story at US News

Call it Mighty Mouse: Breakthrough leaps Alzheimer’s research hurdle

University of California, Irvine researchers have made it possible to learn how key human brain cells respond to Alzheimer’s, vaulting a major obstacle in the quest to understand and one day vanquish it. By developing a way for human brain immune cells known as microglia to grow and function in mice, scientists now have an unprecedented view of crucial mechanisms contributing to the disease.

The team, led by Mathew Blurton-Jones, associate professor of neurobiology & behavior, said the breakthrough also holds promise for investigating many other neurological conditions such as Parkinson’s, traumatic brain injury, and stroke. The details of their study have just been published in the journal Neuron.

The scientists dedicated four years to devising the new rodent model, which is considered “chimeric.” The word, stemming from the mythical Greek monster Chimera that was part goat, lion and serpent, describes an organism containing at least two different sets of DNA.

Full story at Science Daily

Alzheimer’s: Common gene explains why some drugs fail

New insights into a specific gene variant may help to explain why some Alzheimer’s drugs work in certain people but may fail in others. The findings call for a more personalized approach to drug testing.

Earlier this year, a study led by Dr. Kinga Szigeti, Ph.D., who is the director of the Alzheimer’s Disease and Memory Disorders Center at the University of Buffalo, NY, found a key gene that helped explain why some Alzheimer’s drugs showed promise in animal models but failed in humans.

The gene is called CHRFAM7A, and it is specific to humans, although only 75% of people have it. It is a so-called fusion gene — that is, a fusion between a gene that encodes a receptor for the neurotransmitter acetylcholine, and a type of enzyme called a kinase.

Full story at Medical News Today

Coping strategy therapy for family dementia carers works long-term

A programme of therapy and coping strategies for people who care for family members with dementia successfully improves the carers’ mental health for at least a six-year follow-up, finds a UCL study.

Carers who took part in the programme were five times less likely to have clinically significant depression than carers who were not offered the therapy, according to the findings published in the British Journal of Psychiatry.

The intervention has also been shown to be cost-effective in a prior study.

“Taking care of a family member with dementia can be immensely difficult, particularly as their condition deteriorates and they may not appreciate their carer, so close to four in 10 family carers experience depression of anxiety,” said Professor Gill Livingston (UCL Psychiatry), the trial’s principal investigator.

Full story at Science Daily

How having a close relative with Alzheimer’s may affect cognition

New research suggests that having a family history of Alzheimer’s may impair cognition throughout a person’s lifetime, but it also identifies factors that could offset these adverse effects. The findings may enable people at risk to take active measures for delaying or even preventing this form of dementia.

Having a close relative with dementia is a known risk factor for Alzheimer’s disease.

In fact, it is one of the two most significant risk factors, together with age. Having a first-degree relative with Alzheimer’s raises relative risk by 30%, which means that a person’s existing risk goes up by almost a third.

Having a copy of the gene APOE4 that encodes the protein apolipoprotein E raises Alzheimer’s risk by threefold. Having both copies of the gene — which is a rare occurrence — increases the risk by 10 to 15 times.

Full story at Medical News Today

What helps prevent dementia? Try exercise, not vitamin pills

If you want to save your brain, focus on keeping the rest of your body well with exercise and healthy habits rather than popping vitamin pills, new guidelines for preventing dementia advise.

About 50 million people currently have dementia, and Alzheimer’s disease is the most common type. Each year brings 10 million new cases, says the report released Tuesday by the World Health Organization.

Although age is the top risk factor, “dementia is not a natural or inevitable consequence of aging,” it says.

Many health conditions and behaviors affect the odds of developing it, and research suggests that a third of cases are preventable, said Maria Carrillo, chief science officer of the Alzheimer’s Association, which has published similar advice.

Full story at NBC News

Understanding of atrial fibrillation-related dementia

University of Minnesota Medical School researchers have determined that atrial fibrillation (Afib) is independently associated with changes that occur with aging and dementia.

“Atrial Fibrillation and Brain Magnetic Resonance Imaging Abnormalities” published in Stroke advances researchers’ understanding of the mechanisms underlying atrial fibrillation-related dementia. Jeremy Berman, a University of Minnesota cardiology fellow is the first author of this paper. It had already been determined that Afib is associated with dementia independent of clinical stroke but the mechanisms surrounding the association were still unclear.

“Until this point, most studies which looked into this association were cross-sectional, which have limitations,” said Lin Yee Chen, MD, MS, Associate Professor with tenure, Cardiovascular Division, in the Department of Medicine with the University of Minnesota Medical School. “In our study, brain MRI scans were performed at two different times within ten years.”

Full story at Science Daily