The cognitive dysfunction of claustrum on Alzheimer’s disease: A mini-review

• Published in: Frontiers in aging neuroscience Vol. 15; p. 1109256
• Main Authors: Chen, Chun-Yan, Yang, Guang-Yi, Tu, Hai-Xia, Weng, Xu-Chu, Hu, Chun, Geng, Hong-Yan
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 14.04.2023; Frontiers Media S.A
• Subjects: Aging Neuroscience; Alzheimer's disease; Atrophy; Basal ganglia; Brain; claustrum; Cognitive ability; cognitive dysfunction; Dementia disorders; Drug development; Executive function; Memory; Mental disorders; neural circuits; Neurodegenerative diseases; Pathology; Spatial memory; Therapeutic targets; claustrum; pathology; Alzheimer’s disease; cognitive dysfunction; neural circuits
• ISSN: 1663-4365; 1663-4365
• DOI: 10.3389/fnagi.2023.1109256

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases characterized by cognitive deficits and dementia. AD entails predominant pathological characteristics including amyloid beta (Aβ) plaque formation, neurofibrillary entanglements, and brain atrophy, which gradually result in cognitive dysfunctions. Studies showed that these pathological changes are found in a myriad of brain structures, including the claustrum (CLA), a nucleus that penetrates deeply into the brain and is extensively interconnected to various brain structures. The CLA modulates many aspects of cognitive functions, with attention, executive function, visuospatial ability, language, and memory in particular. It is also implicated in multiple neuropsychiatric disorders, of which one worthy of particular attention is AD-related cognitive impairments. To inspire novel AD treatment strategies, this review has summarized the CLA functionality in discriminative cognitive dysfunctions in AD. And then propose an array of potential mechanisms that might contribute to the cognitive impairments caused by an abnormal CLA physiology. We advocate that the CLA might be a new promising therapeutic target in combination with existing anti-AD drugs and brain stimulation approaches for future AD treatment.