Related Experiment Video
Updated: Apr 27, 2026

09:31
Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
Published on: March 7, 2019
9.6K
MS4A Cluster in Alzheimer's Disease
1Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, China.
Molecular Neurobiology
|July 2, 2014
Summary
Genetic variants in the MS4A gene cluster are linked to Alzheimer's disease (AD). These genes, involved in calcium signaling and immunity, may play a role in AD, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- Genome-wide association studies (GWAS) have identified variants in the Membrane-Spanning 4-Domains Subfamily A (MS4A) gene cluster associated with Alzheimer's disease (AD).
- MS4A proteins are cell membrane components involved in calcium signaling, a process relevant to neurodegeneration and AD.
- Several MS4A members (e.g., MS4A1, MS4A2, MS4A4B) have known immune functions, suggesting a broader role for the MS4A cluster in AD pathogenesis.
Purpose of the Study:
- To summarize the structure, localization, and function of the MS4A gene cluster.
- To review recent genetic and expression data linking the MS4A gene cluster to AD.
- To explore the potential roles of the MS4A gene cluster in AD development and progression.
Main Methods:
- Literature review of genetic and expression studies.
- Analysis of existing GWAS data.
- Functional characterization of MS4A family members.
Main Results:
- MS4A gene variants are significantly associated with increased Alzheimer's disease risk.
- MS4A proteins' roles in calcium signaling and immunity suggest mechanisms for AD pathogenesis.
- The MS4A gene cluster represents a promising area for further AD research.
Conclusions:
- The MS4A gene cluster is implicated in Alzheimer's disease pathogenesis through its roles in calcium homeostasis and immune response.
- Targeting the MS4A gene cluster presents a potential novel therapeutic strategy for Alzheimer's disease.
- Further research into MS4A gene function is warranted to fully elucidate its contribution to AD.
Related Concept Videos
Alzheimer Disease ll: Pathophysiology
32
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
32
Alzheimer's Disease: Overview
1.7K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.7K
Alzheimer Disease l: Introduction
20
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
20
Alzheimer's Disease: Treatment
1.3K
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
1.3K
Dementia l: Introduction
31
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
31
Dementia
685
Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual....
The progression of dementia is generally gradual....
685

