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Basic Science and Pathogenesis
Jesus-Adrian Buendia-Meraz1, Maria-Del-Carmen Silva-Lucero1, Juan-Ramon Padilla-Mendoza1,2
1UNAM, School of Medicine, Department of Physiology, CDMX, DF, Mexico.
Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
Summary
Gene editing in familial Alzheimer's disease (FAD) using CRISPR-Cas shows promise. Patient-derived cells exhibited altered maturation, and viral gene correction was successful, though further study is needed to confirm phenotype restoration.
Area of Science:
- Neuroscience
- Genetics
- Cell Biology
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder with sporadic and familial (FAD) forms.
- Gene-editing tools like CRISPR-Cas offer potential for correcting disease-causing mutations.
Purpose of the Study:
- To investigate gene-editing applications for familial Alzheimer's disease.
- To characterize patient-derived cells and assess gene correction efficacy.
Main Methods:
- Cell culture of control and FAD patient-derived neural progenitor cells (NPCs).
- Immunodetection via Western blot and immunocytofluorescence.
- Viral transduction using Adeno-associated viruses (AAV-9) for gene correction.
Main Results:
- FAD-derived NPCs showed increased markers of neuronal differentiation compared to controls.
- Successful viral transduction of patient-derived cells with gene-correction sequences.
- Characterization revealed distinct stem-like and maturation phenotypes between control and FAD cells.
Conclusions:
- FAD patient cells display altered maturation phenotypes.
- Viral gene correction was achieved, but further investigation is required to confirm the restoration of a healthy cellular phenotype.
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