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Updated: Jul 10, 2025
In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology
Annie M Goettemoeller1,2, Emmie Banks1,2, Katharine E McCann3
1Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, 30322.
Early Alzheimer's Disease hyperexcitability in the entorhinal cortex may stem from vulnerable parvalbumin interneurons, not excitatory neurons. Targeting these cells could offer preventative Alzheimer's treatment strategies.
Area of Science:
- Neuroscience
- Cellular Biology
- Alzheimer's Disease Research
Background:
- Alzheimer's Disease (AD) presents early cognitive decline linked to neuronal hyperexcitability.
- Regional vulnerability in early AD, particularly the entorhinal cortex, remains mechanistically unexplained.
- The precise cellular origins of early AD-related hyperexcitability are unknown.
Conclusions:
- Early entorhinal hyperexcitability in Alzheimer's Disease may originate from PV interneurons, challenging previous hypotheses.
- Interventions targeting specific interneuron populations could be a viable preventative strategy for early AD.
- Understanding regional cellular differences is crucial for developing targeted Alzheimer's Disease therapies.
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