ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Contingent vulnerability of entorhinal parvalbumin-containing neurons in Alzheimer's disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Glutamatergic and GABAergic metabolite levels in Alzheimer's disease: a systematic review and meta-analysis.BMC neurology · 2025Pooled it
- Environmental Enrichment Preserves Retrosplenial Parvalbumin Density and Cognitive Function in Female 5xFAD Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Every-Other-Day Feeding Prevents the Loss of Parvalbumin-Expressing Neurons in the Cerebral Cortex of Female 5xFAD Mice.Molecular neurobiology · 2025Article
- Single-nucleus RNA sequencing reveals GABAergic vulnerability and reactive gliosis driven by loss of TDP-43.iScience · 2025Article
- Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer's disease.Science advances · 2025Article
- 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
- Delineating mechanisms underlying parvalbumin neuron impairment in different neurological and neurodegenerative disorders: the emerging role of mitochondrial dysfunction.Biochemical Society transactions · 2024Review
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Alterations of sleep oscillations in Alzheimer's disease: A potential role for GABAergic neurons in the cortex, hippocampus, and thalamus.Brain research bulletin · 2022Review
- Microcircuits for spatial coding in the medial entorhinal cortex.Physiological reviews · 2022Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Inactivation of Presenilin in inhibitory neurons results in decreased GABAergic responses and enhanced synaptic plasticity.Molecular brain · 2021Article
- Cell-autonomous role of Presenilin in age-dependent survival of cortical interneurons.Molecular neurodegeneration · 2020Article
- Distinct disease-sensitive GABAergic neurons in the perirhinal cortex of Alzheimer's mice and patients.Brain pathology (Zurich, Switzerland) · 2020Article
- GABAergic Inhibitory Interneuron Deficits in Alzheimer's Disease: Implications for Treatment.Frontiers in neuroscience · 2020Review
- The basis of cellular and regional vulnerability in Alzheimer's disease.Acta neuropathologica · 2019Review
- The synaptic pathology of cognitive life .Dialogues in clinical neuroscience · 2019Review
- Calcium-Binding Proteins as Determinants of Central Nervous System Neuronal Vulnerability to Disease.International journal of molecular sciences · 2019Review
- Article
- Parvalbumin-Positive Neuron Loss and Amyloid-β Deposits in the Frontal Cortex of Alzheimer's Disease-Related Mice.Journal of Alzheimer's disease : JAD · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-binding proteins containing local circuit neurons are distributed ubiquitously in the human cerebral cortex where they colocalize with a subpopulation of cells that contain GABA. Several reports using a variety of pathological models, including Alzheimer's disease (AD), have suggested that cells containing calcium-binding proteins are resistant to pathological insults. In this report, we test the hypothesis that AD pathology can differentially affect parvalbumin-containing cells depending on their location in the entorhinal cortex and the state of projection neurons with which they are associated. Using cases with different quantities of AD pathology, we determined the density of immunostaining for parvalbumin in the entorhinal cortex, and we correlated this with the concomitant pathological lesions in the various layers of this cortex. Our results show a clear decrease in parvalbumin immunostaining in some parts of the entorhinal cortex when AD neuropathological markers are present. As the density of pathological markers in the entorhinal cortex becomes greater and more widespread, there is a decrease of parvalbumin immunostaining in additional layers, although in all cases, some cells persist. Parvalbumin-containing neurons are clearly vulnerable in AD, but not because of neurofibrillary tangle formation. Instead, they are rendered vulnerable only after substantial loss of projection neurons; only then do they, too, become part of the lesion.
Indexed as
Identifiers
8627368PMC6579156W2144749167What OpenQuestion holds
Registered trials
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.