Cerebral amyloidal angiopathy—A disease with implications for neurology and psychiatry

Gahr, Maximilian; Nowak, Dennis A.; Connemann, Bernhard J.; Schönfeldt‐Lecuona, Carlos

doi:10.1016/j.brainres.2013.04.052

Cited by 39 publications

(37 citation statements)

References 152 publications

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“…Potentially, deposits of amyloid can be found in all tissues. Cerebral amyloid angiopathy (CAA) is characterized by the deposition and accumulation of beta amyloid (Ab) in cerebral vasculature (Gahr et al 2013). The term CAA refers to a heterogenic group of illnesses of the central nervous system, which are characterized histopathologically by the presence of amyloid in the wall of cerebral blood vessels (Biffi & Greenberg 2011;Gahr et al 2013).…”

Section: Introductionmentioning

confidence: 99%

“…CAA in humans can be divided into two forms: hereditary and sporadic. The occurrence of the hereditary (familiar) form is related to various forms of mutations (Thanvi & Robinson 2006;Yamada & Naiki 2012;Gahr et al 2013). The sporadic form occurs much more frequently and mostly as a sporadic condition in the elderly, with an increasing incidence associated with age.…”

Section: Introductionmentioning

confidence: 99%

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Histological and immunohistochemical characteristics of cerebral amyloid angiopathy in elderly dogs

Nešić

Kukolj

Marinković

et al. 2016

Veterinary Quarterly

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Background: Cerebral amyloid angiopathy (CAA) is a disorder characterized by amyloid deposition in the wall of cerebral blood vessels. The deposits of amyloid occur frequently in the blood vessels of the frontal, parietal and occipital cortex. Objective: To examine the characteristics of CAA classified according to the Vonsattel scale in elderly dogs histologically and immunohistochemically as well as the semi-quantitative evaluation of the amyloid deposits in the different segments of the brain. Animals and methods: The brains of 36 dogs of different breeds and sexes, which had been routinely necropsied, were used and divided into two groups: dogs from 1 to 5 and 10 to 18 years old. The tissue sections were stained by hematoxylin-eosin, Congo red and immunohistochemically. Results: Amyloid was accumulated in the wall of cerebral blood vessels in 70% of dogs over the age of 10 years predominantly in the frontal cortex. CAA was demonstrated in elderly dogs as follows: in the frontal cortex (n D 19 or 63%), the parietal cortex (n D 12 or 40%), the hippocampus (40%) and the cerebellum (n D 5 or 17%). The deposits of amyloid in the wall of blood vessels detected by Congo red staining were also Ab1-14 and Ab1-42 immunohistochemically positive. Most commonly, the amyloid deposits affected a moderate number of blood vessels. The accumulation of amyloid was immunohistochemically revealed in the blood vessel walls as well as in the senile plaques and neurons. Conclusion: The amount of amyloid in the arterial walls increased with age in dogs, whereas the amyloid accumulated in plaques was Congo red negative.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Histological and immunohistochemical characteristics of cerebral amyloid angiopathy in elderly dogs

Nešić

Kukolj

Marinković

et al. 2016

Veterinary Quarterly

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“…Sporadic CAA occurs much more frequently and typically in older patients. It occurs in equal frequency in men and women [12].…”

Section: Introductionmentioning

confidence: 99%

“…The only genetic risk factors known for sporadic CAA are apolipoprotein E (ApoE) alleles [12]. The ε2 allele favors CAA-related vascular deterioration (splitting of vascular walls, minor hemorrhaging and fibrinoid necrosis), while the ε4 allele is associated with increased vascular deposition of Aβ.…”

Section: Introductionmentioning

confidence: 99%

“…The ε2 allele favors CAA-related vascular deterioration (splitting of vascular walls, minor hemorrhaging and fibrinoid necrosis), while the ε4 allele is associated with increased vascular deposition of Aβ. Other genetic polymorphisms, such as presenilin 1, α1 antichymotrypsin, neprilysin, oxidized LDL receptors, lipoprotein receptor-related protein, interleukin 33 and transforming growth factor β1, are discussed as possible etiological factors of CAA [12].…”

Section: Introductionmentioning

confidence: 99%

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The development of cerebral amyloid angiopathy in cerebral vessels. A review with illustrations based upon own investigated post mortem cases

Mendel¹,

Wierzba-Bobrowicz²,

Lewandowska³

et al. 2013

pjp

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The process of β-amyloid accumulation in cerebral vessels is presented. Cerebral amyloid angiopathy (CAA) was confirmed during an autopsy. It was diagnosed according to the Boston criteria. Cerebral amyloid angiopathy can involve all kinds of cerebral vessels (cortical and leptomeningeal arterioles, capillaries and veins). The development of CAA is a progressive process. β-amyloid appears first in the tunica media, surrounding smooth muscle cells, and in the adventitia. β-amyloid is progressively accumulated, causing a gradual loss of smooth muscle cells in the vessel wall and finally replacing them. Then, the detachment and delamination of the outer part of the tunica media results in the "double barrel" appearance, fibrinoid necrosis, and microaneurysm formation. Microbleeding with perivascular deposition of erythrocytes and blood breakdown products can also occur. β-amyloid can also be deposited in the surrounding of the affected vessels of the brain parenchyma, known as "dysphoric CAA". Ultrastructurally, when deposits of amyloid fibers were localized in or outside the arteriolar wall, the degenerating vascular smooth muscle cells were observed. In the Institute of Psychiatry and Neurology the study was carried out in a group of 48 patients who died due to intracerebral hemorrhage caused by sporadic CAA.

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Cognition in (pre)symptomatic Dutch‐type hereditary and sporadic cerebral amyloid angiopathy

van Dort,

Kaushik,

Rasing

et al. 2024

Alzheimer's & Dementia

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INTRODUCTIONCerebral amyloid angiopathy (CAA) is a main cause of cognitive dysfunction in the elderly. We investigated specific cognitive profiles, cognitive function in the stage before intracerebral hemorrhage (ICH), and the association between magnetic resonance imaging (MRI) based cerebral small vessel disease (cSVD) burden in CAA because data on these topics are limited.METHODSWe included Dutch‐type hereditary CAA (D‐CAA) mutation carriers with and without ICH, patients with sporadic CAA (sCAA), and age‐matched controls. Cognition was measured with a standardized test battery. Linear regression was performed to assess the association between MRI‐cSVD burden and cognition.RESULTSD‐CAA ICH− mutation carriers exhibited poorer global cognition and executive function compared to age‐matched controls. Patients with sCAA performed worse across all cognitive domains compared to D‐CAA ICH+ mutation carriers and age‐matched controls. MRI‐cSVD burden is associated with decreased processing speed.DISCUSSIONCAA is associated with dysfunction in multiple cognitive domains, even before ICH, with increased MRI‐cSVD burden being associated with slower processing speed.Highlights Cognitive dysfunction is present in early disease stages of cerebral amyloid angiopathy (CAA) before the occurrence of symptomatic intracerebral hemorrhage (sICH). Presymptomatic Dutch‐type CAA (D‐CAA) mutation carriers show worse cognition than age‐matched controls. More early awareness of cognitive dysfunction in CAA before first sICH is needed. Increased cerebral small vessel disease CAA‐burden on magnetic resonance imaging is linked to a decrease in processing speed.

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Cerebral amyloidal angiopathy—A disease with implications for neurology and psychiatry

Cited by 39 publications

References 152 publications

Histological and immunohistochemical characteristics of cerebral amyloid angiopathy in elderly dogs

Histological and immunohistochemical characteristics of cerebral amyloid angiopathy in elderly dogs

The development of cerebral amyloid angiopathy in cerebral vessels. A review with illustrations based upon own investigated post mortem cases

Cognition in (pre)symptomatic Dutch‐type hereditary and sporadic cerebral amyloid angiopathy

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