Pathogenesis of cerebral amyloid angiopathy caused by chaotic glymphatics-Mini-review.
Aβ clearance
aquaporin-4
astrocytes
cerebral amyloid angiopathy
glymphatics
parenchymal border macrophages
Journal
Frontiers in neuroscience
ISSN: 1662-4548
Titre abrégé: Front Neurosci
Pays: Switzerland
ID NLM: 101478481
Informations de publication
Date de publication:
2023
2023
Historique:
received:
05
03
2023
accepted:
27
03
2023
medline:
28
4
2023
pubmed:
28
4
2023
entrez:
28
4
2023
Statut:
epublish
Résumé
Cerebral amyloid angiopathy (CAA) is a common cause of lobar intracerebral hemorrhage in the elderly. It is also associated pathologically with Alzheimer's disease (AD). Both CAA and AD share similar pathology of deposition amyloid beta fibrils (Aβ). Aβ is deposited mainly in the neurites in AD and vascular walls in CAA. Aβ is formed inside the brain parenchyma from the amyloid precursor protein. It is easier to understand how Aβ is deposited in the cerebral neurites in AD. However, the pathogenesis of CAA is still largely unknown. It is difficult to understand or visualize how Aβ fibrils formed inside the brain can be deposited against the cerebral perfusion pressure to be deposited in the cerebral and meningeal arterial walls. We encountered an unusual clinical case of acute aneurysmal subarachnoid hemorrhage which was followed after a few years with localized CAA involving mainly the sites of the subarachnoid hemorrhage. We reviewed the formation of Aβ and postulated how the Aβ fibrils are transported retrogradely toward the cerebral arteries and deposited in the arterial walls resulting in the final pathology of CAA. There is a clear disturbance of the glymphatic system, the aquaporin-4 channel, and the parenchymal border macrophages.
Identifiants
pubmed: 37113157
doi: 10.3389/fnins.2023.1180237
pmc: PMC10126375
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
1180237Informations de copyright
Copyright © 2023 Lui, Alcaide, Knowlton, Ysit and Zhong.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Neuroimage. 2019 Mar;188:616-627
pubmed: 30578928
Sci Transl Med. 2012 Aug 15;4(147):147ra111
pubmed: 22896675
Front Neuroanat. 2017 Nov 07;11:101
pubmed: 29163074
Hirosaki Igaku. 2010 Jul 8;61(Suppl):S111-S124
pubmed: 21037967
Nature. 2022 Nov;611(7936):585-593
pubmed: 36352225
Front Neurosci. 2021 Feb 09;15:639140
pubmed: 33633540
Nat Aging. 2022 Mar;2(3):214-223
pubmed: 36199752
Sci Rep. 2018 May 8;8(1):7194
pubmed: 29740121
Jpn J Radiol. 2021 Jan;39(1):1-14
pubmed: 32653987
J Neurosci. 2013 Nov 13;33(46):18190-9
pubmed: 24227727
Neurol Res Pract. 2021 Jan 19;3(1):5
pubmed: 33499944
Neuron. 2020 Feb 5;105(3):549-561.e5
pubmed: 31810839
Acta Neuropathol. 2016 May;131(5):725-36
pubmed: 26975356
Elife. 2018 Dec 18;7:
pubmed: 30561329
Stroke. 2013 Jun;44(6 Suppl 1):S93-5
pubmed: 23709744
Nat Rev Neurol. 2020 Jan;16(1):30-42
pubmed: 31827267
JCI Insight. 2018 Jul 12;3(13):
pubmed: 29997300
Science. 2013 Oct 18;342(6156):373-7
pubmed: 24136970
Stroke. 2014 Oct;45(10):3092-6
pubmed: 25190438
Alzheimers Dement. 2022 Jan;18(1):10-28
pubmed: 34057813
Front Pharmacol. 2015 Sep 30;6:221
pubmed: 26483691
AJNR Am J Neuroradiol. 2019 Apr;40(4):648-651
pubmed: 30679221
Brain Tumor Pathol. 2016 Apr;33(2):89-96
pubmed: 26920424
Lancet Neurol. 2022 Aug;21(8):714-725
pubmed: 35841910
Ann Neurol. 2014 Dec;76(6):845-61
pubmed: 25204284