AI Article Synopsis
- The first signs of Alzheimer's disease (AD) are cognitive issues linked to problems with synapses.
- The ApoE4 gene is the main risk factor for developing AD later in life and affects how synapses function by disrupting the movement of ApoE receptors.
- A study by Hinrich (2016) reveals that the splicing of ApoE receptor-2 is faulty in brains of people with AD and in mouse models, but fixing this splicing can improve cognitive problems caused by amyloid.
Article Abstract
The earliest clinical manifestation of Alzheimer's disease (AD) is cognitive impairment caused by synaptic dysfunction. ApoE4, the primary risk factor for late‐onset AD, disrupts synaptic homeostasis by impairing synaptic ApoE receptor trafficking. Alternative splicing of ApoE receptor‐2 (Apoer2) maintains synaptic homeostasis. In this issue, Hinrich (2016) show that Apoer2 splicing is impaired in human AD brains and murine AD models and that restoring normal splicing in the mouse rescues amyloid‐induced cognitive defects.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818748 | PMC |
| http://dx.doi.org/10.15252/emmm.201506067 | DOI Listing |
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