ArticleBrain pathology (Zurich, Switzerland)2020
Distinct disease-sensitive GABAergic neurons in the perirhinal cortex of Alzheimer's mice and patients.
Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
- Forced treadmill running and ladder climbing physical activity attenuates cognitive decline and protein aggregates in aged 3xTg-AD mice.Molecular brain · 2026Article
- Depression in neurodegenerative disease: neurobiological mechanisms and emerging treatments.Molecular psychiatry · 2026Review
- Impaired spatial coding and neuronal hyperactivity in the medial entorhinal cortex of aged APP knock-in mice.Cell reports · 2026Article
- Dual platform spatial transcriptomics reveals parvalbumin interneuron subtype vulnerability in mouse models of Alzheimer's disease.Nature communications · 2026Article
- Exploring Linalool-Based Phytotherapy for Excitatory/Inhibitory Imbalance in Alzheimer's Disease: A Review of Lavender and Cannabis Therapeutic Effects on Sleep, Seizures, and Cognition.Phytotherapy research : PTR · 2026Review
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Every-Other-Day Feeding Prevents the Loss of Parvalbumin-Expressing Neurons in the Cerebral Cortex of Female 5xFAD Mice.Molecular neurobiology · 2025Article
- Pathological and Structural Alterations of the Visual Pathway in APP/PS1 Mice: A Spatiotemporal Analysis.Diagnostics (Basel, Switzerland) · 2025Article
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Ligature-induced periodontitis in a transgenic mouse model of Alzheimer's disease dysregulates neuroinflammation, exacerbates cognitive impairment, and accelerates amyloid pathology.Brain, behavior, & immunity - health · 2025Article
- Fast-spiking parvalbumin-positive interneurons: new perspectives of treatment and future challenges in dementia.Molecular psychiatry · 2025Review
- Parvalbumin interneurons in the hippocampal formation of individuals with Alzheimer's disease: a neuropathological study of abnormal phosphorylated tau in neurons.Frontiers in neuroanatomy · 2025Article
- Seizures exacerbate excitatory: inhibitory imbalance in Alzheimer's disease and 5XFAD mice.Brain : a journal of neurology · 2024Article
- Role of GABA pathway in motor and non-motor symptoms in Parkinson's disease: a bidirectional circuit.European journal of medical research · 2024Review
- Sleep disorders cause Parkinson's disease or the reverse is true: Good GABA good night.CNS neuroscience & therapeutics · 2024Review
- Review
- Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer's disease.Molecular psychiatry · 2023Review
- Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Microbiome Alterations and Alzheimer's Disease: Modeling Strategies with Transgenic Mice.Biomedicines · 2023Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal loss is the best neuropathological substrate that correlates with cortical atrophy and dementia in Alzheimer's disease (AD). Defective GABAergic neuronal functions may lead to cortical network hyperactivity and aberrant neuronal oscillations and in consequence, generate a detrimental alteration in memory processes. In this study, using immunohistochemical and stereological approaches, we report that the two major and non-overlapping groups of inhibitory interneurons (SOM-cells and PV-cells) displayed distinct vulnerability in the perirhinal cortex of APP/PS1 mice and AD patients. SOM-positive neurons were notably sensitive and exhibited a dramatic decrease in the perirhinal cortex of 6-month-old transgenic mice (57% and 61% in areas 36 and 35, respectively) and, most importantly, in AD patients (91% in Braak V-VI cases). In addition, this interneuron degenerative process seems to occur in parallel, and closely related, with the progression of the amyloid pathology. However, the population expressing PV was unaffected in APP/PS1 mice while in AD brains suffered a pronounced and significant loss (69%). As a key component of cortico-hippocampal networks, the perirhinal cortex plays an important role in memory processes, especially in familiarity-based memory recognition. Therefore, disrupted functional connectivity of this cortical region, as a result of the early SOM and PV neurodegeneration, might contribute to the altered brain rhythms and cognitive failures observed in the initial clinical phase of AD patients. Finally, these findings highlight the failure of amyloidogenic AD models to fully recapitulate the selective neuronal degeneration occurring in humans.
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