Related Experiment Video
Updated: May 14, 2026
04:22
Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles
Published on: May 20, 2024
TREM2 in Alzheimer's disease.
Teng Jiang1, Jin-Tai Yu, Xi-Chen Zhu
1Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China.
Molecular Neurobiology
|February 15, 2013
Summary
A rare variant in the TREM2 gene increases Alzheimer's disease risk. TREM2 protein may protect against Alzheimer's by reducing inflammation and clearing debris, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- A functional variant (R47H) in the TREM2 gene is linked to late-onset Alzheimer's disease (AD).
- TREM2 protein, encoded by the TREM2 gene, is expressed in brain regions affected by AD.
- Reduced TREM2 function is hypothesized to drive AD pathogenesis.
Purpose of the Study:
- To review epidemiological findings linking TREM2 to late-onset AD.
- To explore the potential roles of TREM2 in AD progression.
- To discuss TREM2 as a therapeutic target for AD.
Main Methods:
- Review of recent epidemiological studies on TREM2 and AD.
- Analysis of TREM2's known functions in microglia.
- Speculation on TREM2's role in AD pathogenesis based on existing evidence.
Main Results:
- The TREM2 R47H variant confers an AD risk comparable to APOE ε4.
- TREM2 appears to suppress microglial inflammatory responses.
- TREM2 is involved in clearing neuronal debris via phagocytosis.
Conclusions:
- TREM2 plays a significant role in AD pathogenesis, potentially through its anti-inflammatory and phagocytic functions.
- Targeting TREM2 presents a promising therapeutic strategy for Alzheimer's disease.
- Further research into TREM2's mechanisms could unlock new AD treatments.
Related Concept Videos
01:23Alzheimer Disease ll: Pathophysiology
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 microglia. Abnormal...
01:26Alzheimer's Disease: Overview
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 and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
01:29Alzheimer Disease l: Introduction
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...
01:22Alzheimer's Disease: Treatment
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...
01:22Dementia l: Introduction
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...
01:24Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...