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Regional alterations of parvalbumin interneurons in human App knock-in mouse model of Alzheimer's disease pathology.

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Τίτλος: Regional alterations of parvalbumin interneurons in human App knock-in mouse model of Alzheimer's disease pathology.
Συγγραφείς: Gonzalez MM; Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, United States. Electronic address: mercgonz@outlook.com., Magondu B; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, United States., Rowan MJM; Department of Cell Biology, Emory University School of Medicine, Atlanta, United States; Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, United States., Forest CR; Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, United States.
Πηγή: Neurobiology of aging [Neurobiol Aging] 2026 Oct; Vol. 166, pp. 41-49. Date of Electronic Publication: 2026 May 15.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Country of Publication: United States NLM ID: 8100437 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1558-1497 (Electronic) Linking ISSN: 01974580 NLM ISO Abbreviation: Neurobiol Aging Subsets: MEDLINE
Imprint Name(s): Publication: New York : Elsevier
Original Publication: Fayetteville, N.Y. : Ankho International.
Ιατρικοί όροι (MeSH): Alzheimer Disease*/pathology , Alzheimer Disease*/metabolism , Alzheimer Disease*/physiopathology , Alzheimer Disease*/genetics , Interneurons*/physiology , Interneurons*/pathology , Interneurons*/metabolism , Parvalbumins*/metabolism , Amyloid beta-Protein Precursor*/genetics , Amyloid beta-Protein Precursor*/metabolism , Entorhinal Cortex*/pathology , Entorhinal Cortex*/cytology , Entorhinal Cortex*/physiopathology , Entorhinal Cortex*/metabolism , Gene Knock-In Techniques*, Visual Cortex/cytology ; Visual Cortex/pathology ; Animals ; Disease Models, Animal ; Humans ; Mice, Transgenic
Περίληψη: Early-stage Alzheimer's disease pathology correlates with disrupted neuronal excitability, which can drive network and cognitive dysfunction even prior to neurodegeneration. However, the emergence and extent of these changes may vary by brain region and cell types situated in those regions. Here we aimed to investigate the effects of Alzheimer's disease pathology on different neuron subtypes in both the entorhinal cortex, a region known to be affected early in Alzheimer's disease, and the primary visual cortex, a relatively unaffected region. We designed and employed a semi-automated patch clamp electrophysiology apparatus to record from fast-spiking parvalbumin interneurons and excitatory neurons in these regions, recording from over 150 cells in 2 month old amyloid precursor protein knock-in (APP-KI) mice. In entorhinal cortex, amyloid overproduction resulted in parvalbumin interneuron hypoexcitability, whereas excitatory neurons were concurrently hyperexcitable. Conversely, neurons of either subclass were largely unaffected in the visual cortex. Together, these findings suggest that fast-spiking parvalbumin interneurons in the entorhinal cortex exhibit selective functional alterations in an early APP-driven state.
(Copyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved.)
Contributed Indexing: Keywords: APP; Alzheimer’s disease; Amyloid precursor protein; Electrophysiology; Interneurons; Parvalbumin
Substance Nomenclature: 0 (Parvalbumins)
0 (Amyloid beta-Protein Precursor)
Entry Date(s): Date Created: 20260525 Date Completed: 20260611 Latest Revision: 20260612
Update Code: 20260612
DOI: 10.1016/j.neurobiolaging.2026.05.005
PMID: 42184608
Βάση Δεδομένων: MEDLINE
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  Data: Regional alterations of parvalbumin interneurons in human App knock-in mouse model of Alzheimer's disease pathology.
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  Data: <searchLink fieldCode="AU" term="%22Gonzalez+MM%22">Gonzalez MM</searchLink>; Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, United States. Electronic address: mercgonz@outlook.com.<br /><searchLink fieldCode="AU" term="%22Magondu+B%22">Magondu B</searchLink>; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, United States.<br /><searchLink fieldCode="AU" term="%22Rowan+MJM%22">Rowan MJM</searchLink>; Department of Cell Biology, Emory University School of Medicine, Atlanta, United States; Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, United States.<br /><searchLink fieldCode="AU" term="%22Forest+CR%22">Forest CR</searchLink>; Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, United States.
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  Data: <searchLink fieldCode="JN" term="%228100437%22">Neurobiology of aging</searchLink> [Neurobiol Aging] 2026 Oct; Vol. 166, pp. 41-49. <i>Date of Electronic Publication: </i>2026 May 15.
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  Data: <i>Publication</i>: New York : Elsevier<br /><i>Original Publication</i>: Fayetteville, N.Y. : Ankho International.
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  Data: <searchLink fieldCode="MM" term="%22Alzheimer+Disease%22">Alzheimer Disease*</searchLink>/<searchLink fieldCode="MM" term="%22Alzheimer+Disease+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Alzheimer+Disease%22">Alzheimer Disease*</searchLink>/<searchLink fieldCode="MM" term="%22Alzheimer+Disease+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Alzheimer+Disease%22">Alzheimer Disease*</searchLink>/<searchLink fieldCode="MM" term="%22Alzheimer+Disease+physiopathology%22">physiopathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Alzheimer+Disease%22">Alzheimer Disease*</searchLink>/<searchLink fieldCode="MM" term="%22Alzheimer+Disease+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Interneurons%22">Interneurons*</searchLink>/<searchLink fieldCode="MM" term="%22Interneurons+physiology%22">physiology</searchLink> <br /><searchLink fieldCode="MM" term="%22Interneurons%22">Interneurons*</searchLink>/<searchLink fieldCode="MM" term="%22Interneurons+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Interneurons%22">Interneurons*</searchLink>/<searchLink fieldCode="MM" term="%22Interneurons+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Parvalbumins%22">Parvalbumins*</searchLink>/<searchLink fieldCode="MM" term="%22Parvalbumins+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Amyloid+beta-Protein+Precursor%22">Amyloid beta-Protein Precursor*</searchLink>/<searchLink fieldCode="MM" term="%22Amyloid+beta-Protein+Precursor+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Amyloid+beta-Protein+Precursor%22">Amyloid beta-Protein Precursor*</searchLink>/<searchLink fieldCode="MM" term="%22Amyloid+beta-Protein+Precursor+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Entorhinal+Cortex%22">Entorhinal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Entorhinal+Cortex+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Entorhinal+Cortex%22">Entorhinal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Entorhinal+Cortex+cytology%22">cytology</searchLink> <br /><searchLink fieldCode="MM" term="%22Entorhinal+Cortex%22">Entorhinal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Entorhinal+Cortex+physiopathology%22">physiopathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Entorhinal+Cortex%22">Entorhinal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Entorhinal+Cortex+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Gene+Knock-In+Techniques%22">Gene Knock-In Techniques*</searchLink><br /><searchLink fieldCode="MH" term="%22Visual+Cortex%22">Visual Cortex</searchLink>/<searchLink fieldCode="MH" term="%22Visual+Cortex+cytology%22">cytology</searchLink> ; <searchLink fieldCode="MH" term="%22Visual+Cortex%22">Visual Cortex</searchLink>/<searchLink fieldCode="MH" term="%22Visual+Cortex+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Disease+Models%2C+Animal%22">Disease Models, Animal</searchLink> ; <searchLink fieldCode="MH" term="%22Humans%22">Humans</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%2C+Transgenic%22">Mice, Transgenic</searchLink>
– Name: Abstract
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  Data: Early-stage Alzheimer's disease pathology correlates with disrupted neuronal excitability, which can drive network and cognitive dysfunction even prior to neurodegeneration. However, the emergence and extent of these changes may vary by brain region and cell types situated in those regions. Here we aimed to investigate the effects of Alzheimer's disease pathology on different neuron subtypes in both the entorhinal cortex, a region known to be affected early in Alzheimer's disease, and the primary visual cortex, a relatively unaffected region. We designed and employed a semi-automated patch clamp electrophysiology apparatus to record from fast-spiking parvalbumin interneurons and excitatory neurons in these regions, recording from over 150 cells in 2 month old amyloid precursor protein knock-in (APP-KI) mice. In entorhinal cortex, amyloid overproduction resulted in parvalbumin interneuron hypoexcitability, whereas excitatory neurons were concurrently hyperexcitable. Conversely, neurons of either subclass were largely unaffected in the visual cortex. Together, these findings suggest that fast-spiking parvalbumin interneurons in the entorhinal cortex exhibit selective functional alterations in an early APP-driven state.<br /> (Copyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved.)
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  Data: <i>Keywords: </i>APP; Alzheimer’s disease; Amyloid precursor protein; Electrophysiology; Interneurons; Parvalbumin
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  Data: 0 (Parvalbumins)<br />0 (Amyloid beta-Protein Precursor)
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  Data: <i>Date Created: </i>20260525 <i>Date Completed: </i>20260611 <i>Latest Revision: </i>20260612
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        Value: 10.1016/j.neurobiolaging.2026.05.005
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      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        StartPage: 41
    Subjects:
      – SubjectFull: Visual Cortex cytology
        Type: general
      – SubjectFull: Visual Cortex pathology
        Type: general
      – SubjectFull: Animals
        Type: general
      – SubjectFull: Disease Models, Animal
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      – SubjectFull: Humans
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      – SubjectFull: Mice, Transgenic
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      – SubjectFull: Alzheimer Disease pathology
        Type: general
      – SubjectFull: Alzheimer Disease metabolism
        Type: general
      – SubjectFull: Alzheimer Disease physiopathology
        Type: general
      – SubjectFull: Alzheimer Disease genetics
        Type: general
      – SubjectFull: Interneurons physiology
        Type: general
      – SubjectFull: Interneurons pathology
        Type: general
      – SubjectFull: Interneurons metabolism
        Type: general
      – SubjectFull: Parvalbumins metabolism
        Type: general
      – SubjectFull: Amyloid beta-Protein Precursor genetics
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      – SubjectFull: Amyloid beta-Protein Precursor metabolism
        Type: general
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      – SubjectFull: Entorhinal Cortex physiopathology
        Type: general
      – SubjectFull: Entorhinal Cortex metabolism
        Type: general
      – SubjectFull: Gene Knock-In Techniques
        Type: general
    Titles:
      – TitleFull: Regional alterations of parvalbumin interneurons in human App knock-in mouse model of Alzheimer's disease pathology.
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              Text: 2026 Oct
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