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A New Piece of the Alzheimer’s Puzzle

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A couple enjoying a hot drink

Credit: National Institute on Aging, NIH

For the past few decades, researchers have been busy uncovering genetic variants associated with an increased risk of Alzheimer’s disease (AD) [1]. But there’s still a lot to learn about the many biological mechanisms that underlie this devastating neurological condition that affects as many as 5 million Americans [2].

As an example, an NIH-funded research team recently found that AD susceptibility may hinge not only upon which gene variants are present in a person’s DNA, but also how RNA messages encoded by the affected genes are altered to produce proteins [3]. After studying brain tissue from more than 450 deceased older people, the researchers found that samples from those with AD contained many more unusual RNA messages than those without AD.


An Aspirin a Day for Older People Doesn’t Prolong Healthy Lifespan

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Hands holding a pill and a glass of water

Credit: iStock/thodonal

Many older people who’ve survived a heart attack or stroke take low-dose aspirin every day to help prevent further cardiovascular problems [1]. There is compelling evidence that this works. But should perfectly healthy older folks follow suit?

Most of us would have guessed “yes”—but the answer appears to be “no” when you consider the latest scientific evidence.  Recently, a large, international study of older people without a history of cardiovascular disease found that those who took a low-dose aspirin daily over more than 4 years weren’t any healthier than those who didn’t. What’s more, there were some unexpected indications that low-dose aspirin might even boost the risk of death.


Alzheimer’s Disease: Tau Protein Predicts Early Memory Loss

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PET imaging of brains affected by Alzheimer's disease

Caption: PET scan images show distribution of tau (top panel) and beta-amyloid (bottom panel) across a brain with early Alzheimer’s disease. Red indicates highest levels of protein binding, dark blue the lowest, yellows and oranges indicate moderate binding.
Credit: Brier et al., Sci Transl Med

In people with Alzheimer’s disease, changes in the brain begin many years before the first sign of memory problems. Those changes include the gradual accumulation of beta-amyloid peptides and tau proteins, which form plaques and tangles that are considered hallmarks of the disease. While amyloid plaques have received much attention as an early indicator of disease, until very recently there hadn’t been any way during life to measure the buildup of tau protein in the brain. As a result, much less is known about the timing and distribution of tau tangles and its relationship to memory loss.

Now, in a study published in Science Translational Medicine, an NIH-supported research team has produced some of the first maps showing where tau proteins build up in the brains of people with early Alzheimer’s disease [1]. The new findings suggest that while beta-amyloid remains a reliable early sign of Alzheimer’s disease, tau may be a more informative predictor of a person’s cognitive decline and potential response to treatment.


LabTV: Young Scientist on a Mission to Cure Alzheimer’s Disease

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Melissa Young LabTV

Time for another LabTV video! Today, I’d like you to meet Melissa Young, a third-year graduate student in the College of Pharmacy, University of Georgia, Athens. Young, who is doing research in the lab of James Franklin, says her scientific goal is to help build the scientific case that oxidative stress plays a key role in Alzheimer’s disease.

Young also has a personal reason for wanting to her research to succeed. From her experiences with a beloved grandmother and aunt, she has seen first-hand the heartbreaking effects of Alzheimer’s disease and other forms of dementia on both patients and their loved ones. Currently, there is no cure for Alzheimer’s disease and no treatments to halt or reverse its progression. That’s one of the reasons why Young has chosen to go into an area of science focused on translating basic discoveries into new therapeutics.


Creative Minds: Opening a Window on Alzheimer’s Before It Strikes

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Yakeel Quiroz

Yakeel Quiroz

While attending college in her native Colombia, Yakeel T. Quiroz joined the Grupo de Neurociencias de Antioquia. This dedicated group of Colombian researchers, healthcare workers, and students has worked for many years with a large extended family in the northwestern district of Antioquia that is truly unique. About half of the more than 5,000 family members inherit a gene mutation that predisposes them to what is known locally as “la bobera,” or “the foolishness,” a devastating form of early-onset Alzheimer’s disease. Those born with the mutation are cognitively healthy through their 20s, become forgetful in their 30s, and descend into full-blown Alzheimer’s disease by their mid-to- late 40s. Making matters worse, multiple family members sometimes are in different stages of dementia at the same time, including the caregiver attempting to hold the household together.

Quiroz, now a researcher at Massachusetts General Hospital in Boston, vowed never to forget these families. She hasn’t, working hard to understand early-onset Alzheimer’s disease and helping to establish the Forget Me Not Initiative to raise money for affected families. With an NIH Director’s Early Independence Award, Quiroz also recently launched her own lab to pursue an even broader scientific opportunity: discover subtle pre-symptomatic changes in the brain years before they give rise to detectable Alzheimer’s. What she learns will have application not only to detect and possibly treat early-onset Alzheimer’s in Colombia but also to understand the late-onset forms of the dementia that affect an estimated 35.6 million people worldwide.


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