scholarly journals Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques

2008 ◽  
Vol 7 ◽  
pp. 67-82 ◽  
Author(s):  
S. Kumar-Singh
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Plaques ◽  
Amyloid Angiopathy ◽  
Pathogenetic Mechanisms ◽  
Cerebral Amyloid

scholarly journals Hereditary cerebral amyloid angiopathy, Piedmont-type mutation

2020 ◽  
Vol 6 (2) ◽  
pp. e411 ◽  
Author(s):  
Mariel G. Kozberg ◽  
Susanne J. van Veluw ◽  
Matthew P. Frosch ◽  
Steven M. Greenberg
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Ex Vivo ◽  
Amyloid Plaques ◽  
Amyloid Angiopathy ◽  
Pathologic Examination ◽  
Potential Association ◽  
History Of ◽  
Intracerebral Hemorrhages ◽  
Β Amyloid ◽  
Cerebral Amyloid

ObjectiveWe present here a case report of a patient with a family history of intracerebral hemorrhages (ICHs) who presented with multiple large lobar hemorrhages in rapid succession, with cognitive sparing, who was found to have a mutation in the β-amyloid coding sequence of amyloid precursor protein (Leu705Val), termed the Piedmont-type mutation, the second ever reported case of this form of hereditary cerebral amyloid angiopathy (CAA).MethodsTargeted pathologic examination was performed aided by the use of ex vivo MRI.ResultsSevere CAA was observed mainly involving the leptomeningeal vessels and, to a far lesser extent, cortical vessels, with no amyloid plaques or neurofibrillary tangles.ConclusionsThis leptomeningeal pattern of β-amyloid deposition coupled with multiple large hemorrhages demonstrates unique pathophysiologic characteristics of CAA associated with the Piedmont-type mutation, suggesting a potential association between leptomeningeal CAA and larger ICHs.

scholarly journals P1-061: Cerebral encephalopathy with cerebral amyloid angiopathy and numerous amyloid plaques presenting aberrant low levels of CSF Aβ 40/1-42

2012 ◽  
Vol 8 (4S_Part_4) ◽  
pp. P127-P128
Author(s):  
Kimitoshi Hirayanagi ◽  
Masaki Ikeda ◽  
Motonobu Arai ◽  
Satoko Kakuda ◽  
Kouki Makioka ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Plaques ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Low Levels

scholarly journals The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy

2019 ◽  
Vol 20 (24) ◽  
pp. 6319 ◽  
Author(s):  
Pablo Cisternas ◽  
Xavier Taylor ◽  
Cristian A. Lasagna-Reeves
Keyword(s):  
Immune Response ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Plaques ◽  
Therapeutic Interventions ◽  
Amyloid Angiopathy ◽  
Clear Understanding ◽  
Major Focus ◽  
Tau Pathology ◽  
Cellular Mechanisms ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there is no clear understanding of the mechanisms underlying the contribution of CAA to neurodegeneration. Despite the fact that CAA is highly associated with the accumulation of Aβ, other types of amyloids have been shown to associate with the vasculature. Interestingly, in many cases, vascular amyloidosis has been associated with an active immune response and perivascular deposition of hyperphosphorylated tau. Despite the fact that in Alzheimer’s disease (AD) a major focus of research has been the understanding of the connection between parenchymal amyloid plaques, tau aggregates in the form of neurofibrillary tangles (NFTs), and immune activation, the contribution of tau and neuroinflammation to neurodegeneration associated with CAA remains understudied. In this review, we discussed the existing evidence regarding the amyloid diversity in CAA and its relation to tau pathology and immune response, as well as the possible contribution of molecular and cellular mechanisms, previously associated with parenchymal amyloid in AD and AD-related dementias, to the pathogenesis of CAA. The detailed understanding of the “amyloid-tau-neuroinflammation” axis in the context of CAA could open the opportunity to develop therapeutic interventions for dementias associated with CAA that are currently being proposed for AD and AD-related dementias.

P3-184: Amyloid plaques, cerebral amyloid angiopathy and cerebral white matter lesions in an autopsy based study

2006 ◽  
Vol 2 ◽  
pp. S428-S429
Author(s):  
Amanda J. Kiliaan ◽  
Lenny van Bon ◽  
Marije C. Gordinou de Gouberville ◽  
Annelieke N. Schepens-Franke ◽  
Pieter J. Dederen ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
White Matter Lesions ◽  
Amyloid Plaques ◽  
Cerebral White Matter ◽  
Amyloid Angiopathy ◽  
Cerebral White Matter Lesions ◽  
Cerebral Amyloid

scholarly journals A Retrospective Study of Canine Senile Plaques and Cerebral Amyloid Angiopathy

1996 ◽  
Vol 33 (2) ◽  
pp. 230-234 ◽  
Author(s):  
T. Yoshino ◽  
K. Uchida ◽  
S. Tateyama ◽  
R. Yamaguchi ◽  
H. Nakayama ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Cerebral Amyloid Angiopathy ◽  
Significant Relationship ◽  
Senile Plaques ◽  
Amyloid Plaques ◽  
Wide Distribution ◽  
Malignant Neoplasms ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Diffuse Plaques

Epidemiologic and morphologic features of canine senile plaques (SPs) and cerebral amyloid angiopathy (CAA) were examined in 69 necropsied dogs. Dogs having only SPs (diffuse plaques) frequently suffered from malignant neoplasms, and their mean age was significantly lower than that of dogs with CAA only. Morphologically, diffuse plaques showed wide distribution compared with amyloid plaques or CAA and were predominantly concentrated in the frontal cortex. We were unable to find any significant relationship between the severity of the SPs and individual age. These findings may indicate that the occurrence of canine SPs is not strictly associated with aging only and that additional factors are related to the occurrence of SPs, especially diffuse plaques.

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