| Literature DB >> 27334648 |
Chenjie Xia1, Bradford C Dickerson1.
Abstract
We have arrived at an exciting juncture in dementia research: the second major pathological hallmark of Alzheimer's disease (AD)-tau-can now be seen for the first time in the living human brain. The major proteinopathies in AD include amyloid-β plaques and neurofibrillary tangles (NFTs) made of hyperphosphorylated paired helical filament (PHF) tau. Since its advent more than a decade ago, amyloid PET imaging has revolutionized the field of dementia research, enabling more confident diagnosis of the likely pathology in patients with a variety of clinical dementia syndromes, paving the way for the identification of people with preclinical or prodromal AD pathology, and serving as a minimally invasive molecular readout in clinical trials of putative disease-modifying interventions. Now that we are on the brink of a second revolution in molecular imaging in dementia, it is worth considering the likely potential impact of this development on the field.Entities:
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Year: 2016 PMID: 27334648 PMCID: PMC5690860 DOI: 10.1017/S1041610216000880
Source DB: PubMed Journal: Int Psychogeriatr ISSN: 1041-6102 Impact factor: 3.878