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Guidelines proposed for newly defined Alzheimer’s-like brain disorder

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Posted May 2, 2019
This news or article is intended for readers with certain scientific or professional knowledge in the field.

A recently recognized brain disorder that mimics clinical features of Alzheimer’s disease has for the first time been defined with recommended diagnostic criteria and other guidelines for advancing and catalyzing future research. Scientists from several National Institutes of Health-funded institutions, in collaboration with international peers, described the newly-named pathway to dementia, Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, in a report published in the journal Brain.

Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, as seen by microscope and MRI. Image credit: Nelson et. al. and Brain, DOI: 10.1093/brain/awz099.

Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, as seen by microscope and MRI. Image credit: Nelson et. al. and Brain, DOI: 10.1093/brain/awz099.

“While we’ve certainly been making advances in Alzheimer’s disease research — such as new biomarker and genetic discoveries—we are still at times asking, ‘When is Alzheimer’s disease not Alzheimer’s disease in older adults?’” said Richard J. Hodes, M.D., director of the National Institute on Aging (NIA), part of the NIH. “The guidance provided in this report, including the definition of LATE, is a crucial step toward increasing awareness and advancing research for both this disease and Alzheimer’s as well.”

Alzheimer’s is the most common form of dementia, which is the loss of cognitive functions — thinking, remembering, and reasoning — and every-day behavioral abilities. In the past, Alzheimer’s and dementia were often considered to be the same. Now there is rising appreciation that a variety of diseases and disease processes contribute to dementia. Each of these diseases appear differently when a brain sample is examined at autopsy. However, it has been increasingly clear that in advanced age, a large number of people had symptoms of dementia without the telltale signs in their brain at autopsy. Emerging research seems to indicate that the protein TDP-43 — though not a stand-alone explanation — contributes to that phenomenon.

Source: NIH

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