Exploring the Impacts of Claustrum on Alzheimer’s Disease

Published on April 14, 2023

Alzheimer’s disease can wreak havoc on the brain, causing cognitive deficits and dementia. One area of interest is the claustrum (CLA), a nucleus deep in the brain that plays a role in various cognitive functions like attention, executive function, visuospatial ability, language, and memory. Recent studies have found that this region is affected by the pathological changes seen in Alzheimer’s disease, such as amyloid beta plaque formation and neurofibrillary entanglements. Understanding how the CLA contributes to cognitive impairments in AD could help develop new treatment strategies. This mini-review explores the functionality of the CLA and proposes potential mechanisms underlying its association with cognitive dysfunction in AD. By targeting the CLA along with existing therapies and brain stimulation techniques, researchers hope to pave the way for more effective treatments for Alzheimer’s disease. Curious to learn more? Dive into the research to uncover the untapped potential of the claustrum!

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.

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