Disrupted astrocyte-neuron signaling reshapes brain activity in epilepsy and Alzheimer’s disease DOI
Mengjie Wu, Ruonan Zhang, Peng Fu

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Deciphering the Functions of Raphe–Hippocampal Serotonergic and Glutamatergic Circuits and their Deficits in Alzheimer’s Disease DOI Open Access
Wanting Yu, R Zhang,

Aosheng Zhang

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(3), P. 1234 - 1234

Published: Jan. 30, 2025

Subcortical innervation of the hippocampus by raphe nucleus is essential for emotional and cognitive control. The two major afferents from to originate serotonergic glutamatergic neurons, which control hippocampal inhibitory network, theta activity, synaptic plasticity have been extensively explored in growing body literature, whereas those circuits received little attention. Notably, both between are disrupted Alzheimer's disease (AD), may contribute initiation progression behavioral psychological symptoms dementia. Thus, deciphering mechanism underlying abnormal raphe-hippocampal AD crucial prevent dementia-associated symptoms. In this review, we summarize anatomical, neurochemical, electrophysiological diversity nuclei as well architecture circuitry. We then elucidate subcortical activity their role regulation emotion cognition. Additionally, present an overview pathogenesis analyze available therapies that can potentially be used clinically alleviate neuropsychiatric decline course.

Language: Английский

Citations

0

Quantification and correlation of amyloid-β plaque load, glial activation, GABAergic interneuron numbers, and cognitive decline in the young TgF344-AD rat model of Alzheimer’s disease DOI Creative Commons

Anett Futácsi,

Kitti Rusznák,

Gergely Szarka

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 12, 2025

Background Animal models of Alzheimer’s disease (AD) are essential tools for investigating pathophysiology and conducting preclinical drug testing. In this study, we examined neuronal glial alterations in the hippocampus medial prefrontal cortex (mPFC) young TgF344-AD rats correlated these changes with cognitive decline amyloid-β plaque load. Methods We compared non-transgenic littermate aged 7–8 months age. systematically quantified β-amyloid plaques, astrocytes, microglia, four different subtypes GABAergic interneurons (calretinin-, cholecystokinin-, parvalbumin-, somatostatin-positive neurons), newly generated neurons hippocampus. Spatial learning memory were assessed using Barnes maze test. Results Young had a large number amyloid plaques both mPFC, together pronounced increase microglial cell numbers. Astrocytic activation was significant mPFC. Cholecystokinin-positive numbers decreased transgenic rats, but calretinin-, not altered. Adult neurogenesis affected by genotype. spatial impairments, deficit did correlate or cellular brain. hippocampus, negatively cholecystokinin-positive neuron astrocytes. Conclusion Pronounced neuropathological found mPFC including loss hippocampal interneurons. Some load, impairment.

Language: Английский

Citations

0

Disrupted astrocyte-neuron signaling reshapes brain activity in epilepsy and Alzheimer’s disease DOI
Mengjie Wu, Ruonan Zhang, Peng Fu

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

0