Neuronal degeneration associated with Alzheimer's disease (AD), is linked to impaired calcium homeostasis and to changes in calcium-binding proteins (CBPs). The AD-related modification of neuronal CBPs remains controversial. Here we analysed the presence and expression of calretinin (CR) and parvalbumin (PV) in the hippocampal CA1 neurones of 18 months old 3xTg-AD mice compared to non-Tg animals. We found a layer specific decrease in number of interneurones expressing CR and PV (by 33.7% and 52%, respectively). Expression of PV decreased (by 13.8%) in PV-positive neurones, whereas expression of CR did not change in CR positive cells. The loss of specific subpopulations of Ca-binding proteins expressing interneurones (CR and PV) together with the decrease of PV in the surviving cells may be linked to their vulnerability to AD pathology. Specific loss of inhibitory interneurones with age could contribute to overall increase in the network excitability associated with AD.
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Article Synopsis
- GABAergic interneurons are crucial for maintaining a balance between excitation and inhibition in the brain, particularly in the prefrontal cortex (PFC); an overload of glucocorticoids, like dexamethasone (DEX), can disrupt these cells and increase vulnerability to mental health issues such as depression and anxiety.
- In a study with adult male mice, chronic DEX treatment led to observed behaviors resembling depression and anxiety, as well as reduced levels of important GABAergic markers and a decrease in brain size and cortex thickness.
- The findings suggest that the decline in GABAergic interneurons due to high DEX exposure may contribute to emotional and behavioral deficits, pointing towards a potential link between glucocorticoid
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