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Groundbreaking Alzheimer’s model in petri dish points to amyloid as disease trigger

NIA-supported researchers recently developed an innovative method to culture human brain cells in the laboratory and then modeled, for the first time, the cascade of cellular changes involved in the onset and progression of Alzheimer’s disease. The findings support the “amyloid hypothesis,” a 30-year-old theory that the build-up of beta-amyloid protein in the brain kick starts the toxic changes that lead to tau tangles, and ultimately, cell death. The results by researchers at Massachusetts General Hospital (MGH), Boston, were published online Oct.

Loss of the sense of smell may predict mortality risk among older people

Frailty and dementia often signal increased risk for mortality among older people. But can the loss of olfaction—the sense of smell—also be a significant indicator of mortality risk? An NIH-supported study involving thousands of older people showed those who could no longer detect or distinguish odors were four times more likely to die within five years than those with normal olfaction. The findings are the first to indicate the importance of olfaction in mortality risk for older adults.

Blog post – oh, what a year it was!

Cartoon of four people in conversation.

During the fiscal year 2014, NIA was affected by a number of events and challenges. As the fiscal year winds down, Dr. Robin Barr, director of the Division of Extramural Activities, looks back on the changes and surprises that occurred, including an expanded research agenda, a budget increase, and an unexpected influx of well-written applications.

Increased brain activity may compensate for amyloid pathology in older brains

Researchers have long wondered why some older people remain cognitively normal despite having abnormal levels of beta-amyloid in their brains, a hallmark of Alzheimer’s disease. While research has shown that older adults with Mild Cognitive Impairment (MCI), which often leads to Alzheimer’s, frequently have increased activity in the hippocampus compared to their cognitively healthy peers, scientists questioned what the hyperactivity represented. Was it helping to compensate for declining brain function or signaling onset of the disease?

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