Related Experiment Video
Updated: Aug 22, 2026

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
Published on: July 6, 2019
Challenges in Studying Synapses in Alzheimer's Disease
1Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA.
None:
Developing therapies for Alzheimer's disease (AD) is a pressing need. A key feature of AD is synapse loss. ApoE4, amyloid-β (Aβ)-peptides, phospho-tau, and neuroinflammation are thought to induce AD pathogenesis, but their molecular mechanisms are incompletely understood. Free Aβ-peptides whose levels decrease in AD are synaptogenic, whereas aggregating Aβ-peptides that accumulate in AD are synaptotoxic. It is unclear whether AD is driven primarily by the loss of free Aβ, the increase of aggregated Aβ, or both, nor do we know how ApoE4 affects synapses. Therefore, understanding the molecular pathways mediating synapse loss in AD is a priority in developing new therapies. ANN NEUROL 2026.
Related Concept Videos
Alzheimer Disease ll: Pathophysiology
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Dementia l: Introduction
Alzheimer Disease l: Introduction
Alzheimer's Disease: Treatment

