ArticleCerebral cortex (New York, N.Y. : 1991)2022
Selective impairment of circuits between prefrontal cortex glutamatergic neurons and basal forebrain cholinergic neurons in a tauopathy mouse model.
Article in Cerebral cortex (New York, N.Y. : 1991), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- The monoaminergic systems as drivers of Alzheimer's disease pathophysiology and symptomatology.Current opinion in neurology · 2026Review
- Compromised synaptic signal from prefrontal cortex to mediodorsal thalamus in Alzheimer's disease models and its rescue by kinase inhibitors.The Journal of physiology · 2026Article
- Synaptic mechanisms for differential severity of social preference deficits in male and female mice induced by diminished activity-dependent BDNF.Frontiers in neuroscience · 2026Article
- Article
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.Neurobiology of disease · 2025Article
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.bioRxiv : the preprint server for biology · 2025Article
- Systemic histone deacetylase inhibition ameliorates the aberrant responses to acute stress in socially isolated male mice.The Journal of physiology · 2024Article
- Gut microbiota metabolites: potential therapeutic targets for Alzheimer's disease?Frontiers in pharmacology · 2024Review
- A sexually dimorphic signature of activity-dependent BDNF signaling on the intrinsic excitability of pyramidal neurons in the prefrontal cortex.Frontiers in cellular neuroscience · 2024Article
- Distinct and Convergent Alterations of Entorhinal Cortical Circuits in Two Mouse Models for Alzheimer's Disease and Related Disorders.Journal of Alzheimer's disease : JAD · 2024Article
- Diminished activity-dependent BDNF signaling differentially causes autism-like behavioral deficits in male and female mice.Frontiers in psychiatry · 2023Article
- Review
- Recent advances in understanding neuronal diversity and neural circuit complexity across different brain regions using single-cell sequencing.Frontiers in neural circuits · 2023Review
- Gut Microbiota Dysbiosis Induced by Decreasing Endogenous Melatonin Mediates the Pathogenesis of Alzheimer's Disease and Obesity.Frontiers in immunology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder linked to cognitive decline. To understand how specific neuronal circuits are impaired in AD, we have used optogenetic and electrophysiological approaches to reveal the functional changes between prefrontal cortex (PFC) and basal forebrain (BF), 2 key regions controlling cognitive processes, in a tauopathy mouse model. We found that the glutamatergic synaptic responses in BF cholinergic neurons from P301S Tau mice (6-8 months old) were markedly diminished. The attenuated long-range PFC to BF pathway in the AD model significantly increased the failure rate of action potential firing of BF cholinergic neurons triggered by optogenetic stimulations of glutamatergic terminals from PFC. In contrast, the projection from PFC to other regions, such as amygdala and striatum, was largely unaltered. On the other hand, optogenetic stimulation of cholinergic terminals from BF induced a persistent reduction of the excitability of PFC pyramidal neurons from Tau mice, instead of the transient reduction exhibited in wild-type mice. Taken together, these data have revealed a selective aberration of the pathway between PFC pyramidal neurons and BF cholinergic neurons in a tauopathy mouse model. This circuit deficit may underlie the loss of attention and executive function in AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.