HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q-Reference-Cited by-同舟云学术

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HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q

Published:2018-10-16 Issue:12 Volume:66 Page:2563-2574
ISSN:0894-1491
Container-title:Glia
language:en
Short-container-title:Glia

Author:

Hammond Jennetta W.¹^ORCID,Qiu Wen Q.¹,Marker Daniel F.¹,Chamberlain Jeffrey M.¹,Greaves-Tunnell Will¹,Bellizzi Matthew J.¹,Lu Shao-Ming¹,Gelbard Harris A.¹

Affiliation:

1. Center for Neurotherapeutics Discovery; University of Rochester Medical Center; Rochester New York

Funder

National Institute of Allergy and Infectious Diseases

National Institute of Mental Health

Publisher

Wiley

Subject

Cellular and Molecular Neuroscience,Neurology

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1002/glia.23511/fullpdf

Reference60 articles.

1. Local self-renewal can sustain CNS microglia maintenance and function throughout adult life;Ajami;Nature Neuroscience,2007

2. Temporal relationships between HIV-1 tat-induced neuronal degeneration, OX-42 immunoreactivity, reactive astrocytosis, and protein oxidation in the rat striatum;Aksenov;Brain Research,2003

3. Programmed cell death in brains of HIV-1-positive AIDS and pre-AIDS patients;An;Acta Neuropathologica,1996

4. Neurotoxicity of HIV-1 proteins gp120 and tat in the rat striatum;Bansal;Brain Research,2000

5. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies;Botto;Nature Genetics,1998

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4. Convergent mechanisms of microglia‐mediated synaptic dysfunction contribute to diverse neuropathological conditions;Annals of the New York Academy of Sciences;2023-06-05

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