Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model
Open accessAbstract
Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown. We studied human amyloid precursor protein (hAPP) transgenic mice, which simulate key aspects of AD. Electroencephalographic recordings in hAPP mice revealed spontaneous epileptiform discharges, indicating network hypersynchrony, primarily during reduced gamma oscillatory activity. Because this oscillatory rhythm is generated by inhibitory parvalbumin (PV) cells, network dysfunction in hAPP mice might arise from impaired PV cells. Supporting this hypothesis, hAPP mice and AD patients had decreased levels of the interneuron-specific and PV cell-predominant voltage-gated sodium channel subunit Nav1.1. Restoring Nav1.1 levels in hAPP mice by Nav1.1-BAC expression increased inhibitory synaptic activity and gamma oscillations and reduced hypersynchrony, memory deficits, and premature mortality. We conclude that reduced Nav1.1 levels and PV cell dysfunction critically contribute to abnormalities in oscillatory rhythms, network synchrony, and memory in hAPP mice and possibly in AD.
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Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.
“Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.15-27”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [24]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAmyloid pathology induces abnormal theta and gamma oscillations, likely due to deficient inhibitory interneuron activity.
“Previous studies show that amyloid pathology induces abnormal theta and gamma oscillations, likely due to deficient inhibitory interneuron activity, not examined here20,49,50.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [50]
The Results section reports abnormal, reduced gamma activity in hAPPJ20 mice, and the Discussion links it to impaired inhibitory PV-cell function. The cited passages do not report abnormal theta oscillations; the findings also come from an amyloid-model mouse study rather than a direct demonstration that amyloid pathology induces both abnormalities. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAmyloid pathology induces abnormal theta and gamma oscillations, likely due to deficient inhibitory interneuron activity.
“Previous studies have shown that amyloid pathology induces abnormal theta and gamma oscillations, likely due to deficient inhibitory interneuron activity”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [48]
The Results section reports abnormal gamma oscillations in hAPPJ20 mice, and the Discussion links reduced gamma activity to dysfunction of inhibitory parvalbumin interneurons. Our copy does not report abnormal theta oscillations; a search for “theta” found no supporting passage. The findings are in an amyloid-related mouse model, rather than a direct demonstration that amyloid pathology induces both rhythms. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAβ-mediated disruptions of glutamate uptake, glutamate release and GABAergic inhibition could explain the hyperexcitability of neurons near Aβ deposits.
“This could be explained by Aβ -mediated disruptions of glutamate uptake 108 , glutamate release 109 and GABAergic inhibition 110 .”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [110]
Perineuronal net structural modification may be related to dysfunctional interneuron activity mediating cognitive impairments in Alzheimer's disease.
“and thus may be related to the dysfunctional interneuron activity mediating cognitive impairments in AD [30, 31].”
From Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain (2020) · cites this paper as [31]
A prevalent hypothesis is that cognitive deficits in Alzheimer's disease are associated with altered activities of FS-PV interneurons.
“A prevalent hypothesis is that cognitive deficits in Alzheimer's disease are associated with altered activities of FS-PV interneurons.31”
From Cortical fast-spiking parvalbumin interneurons enwrapped in the perineuronal net express the metallopeptidases Adamts8, Adamts15 and Neprilysin (2015) · cites this paper as [31]
Restoring Nav1.1 levels increased gamma oscillations and reduced memory deficits and premature deaths.
“Restoration of the levels of this voltage-gated sodium channel increased gamma oscillations, while memory deficits and premature deaths decreased [26].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [26]
Nav1.1, a voltage-gated sodium channel found largely on PV-IN axons, is decreased in a mouse model with amyloid pathology and in AD patients.
“Separately, a voltage-gated sodium channel (Na v 1.1) that is largely found on axons of PV-INs was decreased in a mouse model with amyloid pathology, and in AD patients [24][25][26].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [26]
Reduced Nav1.1 levels and PV-containing interneuron dysfunction critically contribute to abnormalities in oscillations, synchrony, and memory in human amyloid precursor protein transgenic mice and possibly in humans with Alzheimer's disease.
“Reduced Nav1.1 levels and PV-containing interneuron dysfunction critically contribute to abnormalities in oscillations, synchrony, and memory in human amyloid precursor protein transgenic mice and possibly in humans with Alzheimers disease (1170).”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1170]
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BackgroundInfluentialFunctional fission of parvalbumin interneuron classes during fast network events
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- Authors
- Verret, L., Mann, E. O., Hang, G. B., Barth, A. M. I., Cobos, I., Ho, K., Devidze, N., Masliah, E., Kreitzer, A. C., Mody, I., Mucke, L., & Palop, J. J.
- Affiliations
- Gladstone Institutes (US)
- University of California, Los Angeles (US)
- University of California, San Francisco (US)
- University of California San Diego (US)
- Corresponding author
- Palop, Jorge J.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 149
- Issue
- 3
- Pages
- 708-721
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3375906
- OpenAlex
- W1979612107
- Cited by
- 1,216
- References
- 59
- Citations by year
- 2026: 101 · 2025: 113 · 2024: 114 · 2023: 86 · 2022: 116 · 2021: 125 · 2020: 93 · 2019: 87 · 2018: 71 · 2017: 66 · 2016: 66 · 2015: 54 · 2014: 61 · 2013: 48 · 2012: 14
- FWCI
- 37.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute on Aging (AG011385, R37AG018440, R37AG011385, R01AG018440, P50AG005131, AG-5131, AG022074, AG 18440, P01AG022074, R01AG011385)
- National Institute of Neurological Disorders and Stroke (P01NS002808, NS-030549, NS065780, P30NS065780, R37NS030549, R01NS030549, NS 002808)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- Alzheimer's disease, inhibitory interneurons, Nav1.1 sodium channel, gamma oscillations, epileptiform discharges, memory impairment, cognitive impairment
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Humans, Interneurons, Learning, Memory, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Neurons, Synapses, Sodium Channels, Amyloid beta-Protein Precursor, Mice, NAV1.1 Voltage-Gated Sodium Channel, In Vitro Techniques
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