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Parvalbumin Interneuron Dysfunction in Neurological Disorders: Focus on Epilepsy and Alzheimer's Disease
1Department of Anatomy, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin 9016, New Zealand.
International Journal of Molecular Sciences
|May 25, 2024
Summary
Dysfunctional parvalbumin (PV+) interneurons disrupt brain excitation/inhibition balance, causing seizures and cognitive decline. Targeting these neurons offers therapeutic potential for epilepsy and Alzheimer's disease (AD).
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Systems Neuroscience
Background:
- Parvalbumin-expressing (PV+) GABAergic interneurons are crucial for brain function, regulating excitation and synchrony.
- Their dysfunction is linked to hyperexcitability, seizures, and cognitive impairments, particularly in aging and Alzheimer's disease (AD).
Purpose of the Study:
- To review the role of dysfunctional PV+ interneurons in epilepsy and cognitive decline.
- To explore PV+ interneurons as therapeutic targets for neurological disorders.
Main Methods:
- Review of existing literature on PV+ interneuron function and dysfunction.
- Discussion of recent optogenetic and chemogenetic studies manipulating PV+ interneurons in animal models.
Main Results:
- PV+ interneuron deficits disrupt excitatory/inhibitory balance, contributing to seizures and cognitive impairment.
- Selective manipulation of PV+ interneurons can control seizures and restore neural activity balance in animal models.
Conclusions:
- Dysfunctional PV+ interneurons are implicated in epilepsy and cognitive decline, including AD.
- Targeting PV+ interneurons presents a promising therapeutic strategy for these conditions.
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