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Profound degeneration of wake‐promoting neurons in Alzheimer's disease
Author(s) -
Oh Jun,
Eser Rana A.,
Ehrenberg Alexander J.,
Morales Dulce,
Petersen Cathrine,
Kudlacek Jessica,
Dunlop Sara R.,
Theofilas Panos,
Resende Elisa D.P.F.,
Cosme Celica,
Alho Eduardo J.L.,
Spina Salvatore,
Walsh Christine M.,
Miller Bruce L.,
Seeley William W.,
Bittencourt Jackson C.,
Neylan Thomas C.,
Heinsen Helmut,
Grinberg Lea T.
Publication year - 2019
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2019.06.3916
Subject(s) - wake , degeneration (medical) , neuronal degeneration , disease , neuroscience , alzheimer's disease , medicine , psychology , pathology , physics , mechanics
Sleep‐wake disturbances are a common and early feature in Alzheimer's disease (AD). The impact of early tau pathology in wake‐promoting neurons (WPNs) remains unclear. Methods We performed stereology in postmortem brains from AD individuals and healthy controls to identify quantitative differences in morphological metrics in WPNs. Progressive supranuclear palsy (PSP) and corticobasal degeneration were included as disease‐specific controls. Results The three nuclei studied accumulate considerable amounts of tau inclusions and showed a decrease in neurotransmitter‐synthetizing neurons in AD, PSP, and corticobasal degeneration. However, substantial neuronal loss was exclusively found in AD. Discussion WPNs are extremely vulnerable to AD but not to 4 repeat tauopathies. Considering that WPNs are involved early in AD, such degeneration should be included in the models explaining sleep‐wake disturbances in AD and considered when designing a clinical intervention. Sparing of WPNs in PSP, a condition featuring hyperinsomnia, suggest that interventions to suppress the arousal system may benefit patients with PSP.