Alzheimer disease

David S. Knopman; Helene Amieva; Ronald C. Petersen; Gäel Chételat; David M. Holtzman; Bradley T. Hyman; Ralph A. Nixon; David T. Jones

doi:10.1038/s41572-021-00269-y

Alzheimer disease

David S. Knopman, Helene Amieva, Ronald C. Petersen, Gäel Chételat, David M. Holtzman, Bradley T. Hyman, Ralph A. Nixon, David T. Jones

Research output: Contribution to journal › Article › peer-review

Abstract

Alzheimer disease (AD) is biologically defined by the presence of β-amyloid-containing plaques and tau-containing neurofibrillary tangles. AD is a genetic and sporadic neurodegenerative disease that causes an amnestic cognitive impairment in its prototypical presentation and non-amnestic cognitive impairment in its less common variants. AD is a common cause of cognitive impairment acquired in midlife and late-life but its clinical impact is modified by other neurodegenerative and cerebrovascular conditions. This Primer conceives of AD biology as the brain disorder that results from a complex interplay of loss of synaptic homeostasis and dysfunction in the highly interrelated endosomal/lysosomal clearance pathways in which the precursors, aggregated species and post-translationally modified products of Aβ and tau play important roles. Therapeutic endeavours are still struggling to find targets within this framework that substantially change the clinical course in persons with AD.

Original language	English (US)
Article number	33
Journal	Nature Reviews Disease Primers
Volume	7
Issue number	1
DOIs	https://doi.org/10.1038/s41572-021-00269-y
State	Published - Dec 2021

ASJC Scopus subject areas

General Medicine

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10.1038/s41572-021-00269-y

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title = "Alzheimer disease",

abstract = "Alzheimer disease (AD) is biologically defined by the presence of β-amyloid-containing plaques and tau-containing neurofibrillary tangles. AD is a genetic and sporadic neurodegenerative disease that causes an amnestic cognitive impairment in its prototypical presentation and non-amnestic cognitive impairment in its less common variants. AD is a common cause of cognitive impairment acquired in midlife and late-life but its clinical impact is modified by other neurodegenerative and cerebrovascular conditions. This Primer conceives of AD biology as the brain disorder that results from a complex interplay of loss of synaptic homeostasis and dysfunction in the highly interrelated endosomal/lysosomal clearance pathways in which the precursors, aggregated species and post-translationally modified products of Aβ and tau play important roles. Therapeutic endeavours are still struggling to find targets within this framework that substantially change the clinical course in persons with AD.",

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AU - Knopman, David S.

AU - Amieva, Helene

AU - Petersen, Ronald C.

AU - Chételat, Gäel

AU - Holtzman, David M.

AU - Hyman, Bradley T.

AU - Nixon, Ralph A.

AU - Jones, David T.

PY - 2021/12

Y1 - 2021/12

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AB - Alzheimer disease (AD) is biologically defined by the presence of β-amyloid-containing plaques and tau-containing neurofibrillary tangles. AD is a genetic and sporadic neurodegenerative disease that causes an amnestic cognitive impairment in its prototypical presentation and non-amnestic cognitive impairment in its less common variants. AD is a common cause of cognitive impairment acquired in midlife and late-life but its clinical impact is modified by other neurodegenerative and cerebrovascular conditions. This Primer conceives of AD biology as the brain disorder that results from a complex interplay of loss of synaptic homeostasis and dysfunction in the highly interrelated endosomal/lysosomal clearance pathways in which the precursors, aggregated species and post-translationally modified products of Aβ and tau play important roles. Therapeutic endeavours are still struggling to find targets within this framework that substantially change the clinical course in persons with AD.

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Alzheimer disease

Abstract

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