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Trends Mol Med. 2017 Jun;23(6):534-545. doi: 10.1016/j.molmed.2017.04.001. Epub 2017 May 5.

The Exceptional Vulnerability of Humans to Alzheimer's Disease.

Author information

1
Department of Neurology and Yerkes National Primate Research Center, Emory University, Atlanta, GA 30322, USA. Electronic address: lary.walker@emory.edu.
2
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, and the German Center for Neurodegenerative Diseases (DZNE), D-72076 Tübingen, Germany. Electronic address: mathias.jucker@uni-tuebingen.de.

Abstract

Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age. Nevertheless, the complete behavioral and pathologic phenotype of Alzheimer's disease, including Aβ plaques, neurofibrillary (tau) tangles, and dementia, has not yet been identified in a non-human species. Recent research suggests that the crucial link between Aβ aggregation and tauopathy is somehow disengaged in aged monkeys. Understanding why Alzheimer's disease fails to develop in species that are biologically proximal to humans could disclose new therapeutic targets in the chain of events leading to neurodegeneration and dementia.

KEYWORDS:

Aβ; aging; amyloid; dementia; neurodegeneration; non-human primate; prion; proteopathy; seeding; tau

PMID:
28483344
PMCID:
PMC5521004
DOI:
10.1016/j.molmed.2017.04.001
[Indexed for MEDLINE]
Free PMC Article

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