Neurobiologic Rationale for Treatment of Apathy in Alzheimer's Disease With Methylphenidate.
Alzheimer's disease
apathy
catecholamines
dopamine
methylphenidate
norepinephrine
prefrontal cortex
Journal
The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry
ISSN: 1545-7214
Titre abrégé: Am J Geriatr Psychiatry
Pays: England
ID NLM: 9309609
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
04
02
2020
revised:
28
04
2020
accepted:
29
04
2020
pubmed:
29
5
2020
medline:
4
8
2021
entrez:
29
5
2020
Statut:
ppublish
Résumé
The public health burden of Alzheimer's disease (AD) is related not only to cognitive symptoms, but also to neuropsychiatric symptoms, including apathy. Apathy is defined as a quantitative reduction of goal-directed activity in comparison to a previous level of functioning and affects 30%-70% of persons with AD. Previous attempts to treat apathy in AD-both nonpharmacologically and pharmacologically-have been wanting. Catecholaminergic treatment with methylphenidate has shown encouraging results in initial trials of apathy in AD. Understanding the neuronal circuits underlying motivated behavior and their reliance on catecholamine actions helps provide a rationale for methylphenidate actions in the treatment of apathy in patients with AD. Anatomical, physiological, and behavioral studies have identified parallel, cortical-basal ganglia circuits that govern action, cognition, and emotion and play key roles in motivated behavior. Understanding the distinct contributions to motivated behavior of subregions of the prefrontal cortex-dorsolateral, orbital-ventromedial, and dorsomedial-helps to explain why degeneration of these areas in AD results in apathetic behaviors. We propose that the degeneration of the prefrontal cortex in AD produces symptoms of apathy. We further propose that methylphenidate treatment may ameliorate those symptoms by boosting norepinephrine and dopamine actions in prefrontal-striatal-thalamocortical circuits.
Identifiants
pubmed: 32461027
pii: S1064-7481(20)30327-4
doi: 10.1016/j.jagp.2020.04.026
pmc: PMC7641967
mid: NIHMS1598370
pii:
doi:
Substances chimiques
Methylphenidate
207ZZ9QZ49
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
51-62Subventions
Organisme : NIA NIH HHS
ID : P30 AG066507
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG066508
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG047270
Pays : United States
Organisme : RRD VA
ID : I01 RX002638
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG046543
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
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