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Alzheimer's Disease: Treatment

Alzheimer'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...

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Related Experiment Video

Updated: Apr 3, 2026

Isolation and Direct Neuronal Reprogramming of Mouse Astrocytes

Isolation and Direct Neuronal Reprogramming of Mouse Astrocytes

Published on: July 7, 2022

Reprogramming aging astrocytes in Alzheimer's disease.

Maria Alfonso-Triguero¹, Amaia M Arranz²

¹Achucarro Basque Center for Neuroscience, Leioa, Spain; Department of Neurosciences, University of the Basque Country (UPV/EHU), Leioa, Spain.

Trends in Neurosciences

|April 2, 2026

Summary

This summary is machine-generated.

Researchers found that restoring a specific gene pathway in aging astrocytes can clear amyloid plaques and improve memory in mice with Alzheimer's disease. This suggests that astrocyte dysfunction in aging brains may be reversible.

Keywords:

MEGF10 Sox9 amyloid-β clearance circuit function glial plasticity transcriptional regulation

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Area of Science:

Neuroscience
Molecular Biology
Aging Research

Background:

Alzheimer's disease is linked to aging brain changes, including altered astrocyte function.
Astrocytic transcriptional programs undergo significant remodeling during brain aging.

Purpose of the Study:

To investigate the role of the Sox9-MEGF10 axis in aging-related astrocyte dysfunction.
To determine if restoring this axis can ameliorate Alzheimer's-like pathology and cognitive deficits in mouse models.

Main Methods:

Utilized mouse models of Alzheimer's disease.
Focused on manipulating the SRY-box transcription factor 9 (Sox9) and multiple EGF-like domains 10 (MEGF10) pathway in astrocytes.
Assessed amyloid-beta clearance and cognitive function.

Main Results:

Reinstating the aging-dependent Sox9-MEGF10 axis restored amyloid clearance in the brain.
Preservation of cognitive function was observed in treated mouse models.
Demonstrated that astrocyte dysfunction in aging is not necessarily irreversible.

Conclusions:

Astrocyte dysfunction in aging brains, while destabilized, represents a recoverable homeostatic program.
Targeting the Sox9-MEGF10 axis offers a potential therapeutic strategy for Alzheimer's disease by rejuvenating astrocyte function.