Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer’s pathology

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: 1 Online-Ressource.

Language: Englisch

Bibliographic citation: Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer’s pathology ; volume:15 ; number:1 ; day:1 ; month:4 ; year:2024 ; pages:1-26 ; date:12.2024
Nature Communications ; 15, Heft 1 (1.4.2024), 1-26, 12.2024

Creator: Kumar, Prateek
Goettemoeller, Annie M.
Espinosa-Garcia, Claudia
Tobin, Brendan R.
Tfaily, Ali
Nelson, Ruth S.
Natu, Aditya
Dammer, Eric B.
Santiago, Juliet V.
Malepati, Sneha
Cheng, Lihong
Xiao, Hailian
Duong, Duc D.
Seyfried, Nicholas T.
Wood, Levi B.
Rowan, Matthew J. M.
Rangaraju, Srikant

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41467-024-47028-7

URN: urn:nbn:de:101:1-2406181254207.908474770695

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:59 AM CEST

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Kumar, Prateek
Goettemoeller, Annie M.
Espinosa-Garcia, Claudia
Tobin, Brendan R.
Tfaily, Ali
Nelson, Ruth S.
Natu, Aditya
Dammer, Eric B.
Santiago, Juliet V.
Malepati, Sneha
Cheng, Lihong
Xiao, Hailian
Duong, Duc D.
Seyfried, Nicholas T.
Wood, Levi B.
Rowan, Matthew J. M.
Rangaraju, Srikant
SpringerLink (Online service)

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Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer’s pathology

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Other Objects (12)

Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease

Optogenetic silencing of Parvalbumin-expressing hippocampal interneurons

Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

Loss of LAMP5 interneurons drives neuronal network dysfunction in Alzheimer’s disease

Parvalbumin-expressing interneurons in the medial entorhinal cortex

Intersectional strategy to study cortical inhibitory parvalbumin-expressing interneurons

DOT1L deletion impairs the development of cortical parvalbumin-expressing interneurons

Network-driven plasma proteomics expose molecular changes in the Alzheimer’s brain

Experimentally constrained network model of hippocampal fast-firing parvalbumin-positive interneurons

Discrete hippocampal projections are differentially regulated by parvalbumin and somatostatin interneurons

Multiplex proteomics identifies novel CSF and plasma biomarkers of early Alzheimer’s disease

Potential prognostic value of CSF-targeted proteomics across the Alzheimer’s disease continuum

Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease

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Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

Loss of LAMP5 interneurons drives neuronal network dysfunction in Alzheimer’s disease

Parvalbumin-expressing interneurons in the medial entorhinal cortex

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DOT1L deletion impairs the development of cortical parvalbumin-expressing interneurons

Network-driven plasma proteomics expose molecular changes in the Alzheimer’s brain

Experimentally constrained network model of hippocampal fast-firing parvalbumin-positive interneurons

Discrete hippocampal projections are differentially regulated by parvalbumin and somatostatin interneurons

Multiplex proteomics identifies novel CSF and plasma biomarkers of early Alzheimer’s disease

Potential prognostic value of CSF-targeted proteomics across the Alzheimer’s disease continuum

Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease

Optogenetic silencing of Parvalbumin-expressing hippocampal interneurons

Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

Loss of LAMP5 interneurons drives neuronal network dysfunction in Alzheimer’s disease

Parvalbumin-expressing interneurons in the medial entorhinal cortex

Intersectional strategy to study cortical inhibitory parvalbumin-expressing interneurons

DOT1L deletion impairs the development of cortical parvalbumin-expressing interneurons

Network-driven plasma proteomics expose molecular changes in the Alzheimer’s brain

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Discrete hippocampal projections are differentially regulated by parvalbumin and somatostatin interneurons

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