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Mechanisms of memory impairment in animal models of nontraumatic intracranial hemorrhage: A systematic review of the literature.

作者信息

Peterson Catherine, Umoye Alexis O, Puglisi Chloe H, Waldau Ben

机构信息

Department of Neurological Surgery, University of California Davis, 4860 Y St., Suite 3740, Sacramento, CA 95817, United States.

出版信息

Brain Hemorrhages. 2022 Jun;3(2):77-93. doi: 10.1016/j.hest.2021.08.002. Epub 2021 Aug 10.


DOI:10.1016/j.hest.2021.08.002
PMID:36093312
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9454327/
Abstract

Mechanisms underlying memory and cognitive dysfunction following spontaneous intracranial hemorrhage are diverse. The aim of this systematic review was to provide a contemporary review of the commonly reported mechanisms responsible for memory impairment following nontraumatic intracranial hemorrhage. PubMed, Embase, and Scopus databases were systematically searched for pre-clinical studies, and results were reported according to PRISMA guidelines. Methodological quality assessment was performed according to the SYRCLE's Risk of Bias tool. Ninety studies met the inclusion criteria. Most of animal studies reported on subarachnoid hemorrhage (48%), followed by intraparenchymal hemorrhage (44%), and intraventricular hemorrhage (8%). Most of subarachnoid hemorrhage studies (30%) reported neuronal apoptosis as a mechanism for memory dysfunction, whereas the most commonly described mechanism following intraparenchymal hemorrhage (40%) and intraventricular hemorrhage (23%) was a proinflammatory response. Based on SYRCLE's Risk of Bias assessment, the average methodological risk of bias of all studies was 56.83 ± 12.77% on a 0-100% scale. There is a great need not only for more preclinical studies with improved methodology, but also for studies reporting negative treatment effects and for multicenter animal studies. In vivo studies on non-rodent animal ICH models can also be helpful.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/d05fe72c7b82/nihms-1834561-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/4208e6a7a3d5/nihms-1834561-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/590732ed416c/nihms-1834561-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/965599f097e9/nihms-1834561-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/ed86458b69f8/nihms-1834561-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/49da9f6267c3/nihms-1834561-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/22349bffe7a4/nihms-1834561-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/d05fe72c7b82/nihms-1834561-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/4208e6a7a3d5/nihms-1834561-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/590732ed416c/nihms-1834561-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/965599f097e9/nihms-1834561-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/ed86458b69f8/nihms-1834561-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/49da9f6267c3/nihms-1834561-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/22349bffe7a4/nihms-1834561-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4385/9454327/d05fe72c7b82/nihms-1834561-f0007.jpg

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本文引用的文献

[1]
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Neurobiol Dis. 2020-11

[2]
Subarachnoid hemorrhage leads to early and persistent functional connectivity and behavioral changes in mice.

J Cereb Blood Flow Metab. 2021-5

[3]
Galectin-9 Promotes Neuronal Restoration via Binding TLR-4 in a Rat Intracerebral Hemorrhage Model.

Neuromolecular Med. 2021-6

[4]
Hydrogen Sulfide Reduces Cognitive Impairment in Rats After Subarachnoid Hemorrhage by Ameliorating Neuroinflammation Mediated by the TLR4/NF-κB Pathway in Microglia.

Front Cell Neurosci. 2020-7-9

[5]
Astrocytic histone deacetylase 2 facilitates delayed depression and memory impairment after subarachnoid hemorrhage by negatively regulating glutamate transporter-1.

Ann Transl Med. 2020-6

[6]
Activated WNK3 induced by intracerebral hemorrhage deteriorates brain injury maybe via WNK3/SPAK/NKCC1 pathway.

Exp Neurol. 2020-10

[7]
Long-term outcomes of monascin - a novel dual peroxisome proliferator-activated receptor γ/nuclear factor-erythroid 2 related factor-2 agonist in experimental intracerebral hemorrhage.

Ther Adv Neurol Disord. 2020-5-14

[8]
Long-term chemogenetic activation of M1 glutamatergic neurons attenuates the behavioral and cognitive deficits caused by intracerebral hemorrhage.

Biochem Biophys Res Commun. 2020-6-18

[9]
Neuroprotective potential of solanesol in a combined model of intracerebral and intraventricular hemorrhage in rats.

IBRO Rep. 2020-4-22

[10]
Nix Plays a Neuroprotective Role in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats.

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