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They emphasized that the "oldest-old" are at greatest risk, and they believe that the public health impact of LATE is at least as large as Alzheimer's in this group.The clinical and neurocognitive features of LATE affect multiple areas of cognition, ultimately impairing activities of daily life.
Now there is growing appreciation that a variety of diseases and disease processes contribute to dementia with memory loss.
Each of these diseases appears differently in brain samples examined at autopsy of people who died with these conditions.
"As we continue to make large strides in our understanding of memory loss and dementia in aging, we have renewed confidence that we will be able to work towards a more individualized approach to preventions and treatments," said Schneider.
Funding included grants from NIH: U01AG016976, P01AG003949, R01AG03749, P50AG016574, R01AG054449, P30AG028303, P30AG012300, P30AG049638, P30AG010124, P30AG010161, P50AG047366, P50AG025688, P50AG005131, R37AG011378, R01AG041851, R01AG042210, R01AG017917, R01AG034374, UF1AG053983 and UF1AG057707. "Researchers define Alzheimer's-like brain disorder: LATE symptoms resembles Alzheimer's disease but has different cause." Science Daily. The accumulation of beta-Amyloid and tau proteins in the brain is hallmark pathology for Alzheimer disease.
As more cells die, Alzheimer's disease continues to progress.
Experts are cautiously hopeful about developing Alzheimer's treatments that can stop or significantly delay the progression of Alzheimer's.Suggestions were provided for possible strategies to help guide future therapeutic interventions, including the importance of removing subjects with LATE from clinical trials of Alzheimer's treatments, which could significantly improve the chances of successful Alzheimer's breakthroughs.The researchers also discussed the importance of more epidemiological, clinical, neuroimaging and genetic studies to better characterize LATE, and the need for research in diverse populations.'Oldest old' are at greatest risk of LATE It has become increasingly clear that in advanced age, a large number of people had symptoms of dementia without the telltale signs of Alzheimer's disease in their brains at autopsy.Emerging research seems to indicate that TDP-43, while not a stand-alone explanation, is a large contributor to that phenomenon.The function of normal TDP-43 (transactive response DNA binding protein of 43 k Da) is related to how cells use DNA to make proteins.In disease, TDP protein becomes misfolded (abnormally structured) and moves from its normal location in the cell.A brain disorder that mimics symptoms of Alzheimer's disease has been defined with recommended diagnostic criteria and guidelines for advancing future research on the condition.Researchers at Rush University Medical Center and 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 today in the journal "We proposed a new name to increase recognition and research for this common cause of dementia, the symptoms of which mimic Alzheimer's dementia but is not caused by plaques and tangles (the buildup of beta amyloid proteins that Alzheimer's produces).Submitted papers should be no more than 5 pages and specifically should address one or more of the following issues: APS Fellow Wendy Wood and APS William James Fellow Timothy D.Wilson offer a behind-the-scenes look at the recent National Academies of Sciences, Engineering, and Medicine report on reproducibility and replicability in science.