Differences between the Pathogenesis of Senile Plaques and Congophilic Angiopathy in Alzheimer Disease

Verbeek, Marcel M.; Eikelenboom, Piet; Waal, R.M.W. de

doi:10.1097/00005072-199707000-00001

Cited by 15 publications

(18 citation statements)

References 33 publications

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“…Furthermore, these data are in line with our previously proposed hypothesis that the pathogenesis of CAA and senile plaques is different, e.g. with respect to the involvement of Aβ‐associated proteins [41]. Finally, the exact role of sHsps in the deposition, aggregation or clearance of Aβ in AD brains needs further elucidation but may provide a target for interference with this disease.…”

Section: Discussionsupporting

confidence: 88%

Specific association of small heat shock proteins with the pathological hallmarks of Alzheimer's disease brains

Wilhelmus

Otte-Höller²,

Wesseling³

et al. 2006

Neuropathology Appl Neurobio

202

157

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The small heat shock protein family (sHsp) comprises molecular chaperones able to interact with incorrectly folded proteins. Alzheimer's disease (AD) is characterized by pathological lesions such as senile plaques (SPs), cerebral amyloid angiopathy (CAA) and neurofibrillary tangles (NFTs), predominantly consisting of the incorrectly folded proteins amyloid-beta (Abeta) and tau respectively. The aim of this study was to investigate the association of the chaperones Hsp20, HspB2, alphaB-crystallin and Hsp27 with the pathological lesions of AD brains. For this purpose, a panel of well-characterized antibodies directed against these sHsps was used in immunohistochemistry and immunoblotting. We observed extracellular expression of Hsp20, Hsp27 and HspB2 in classic SPs, and Hsp20 expression in diffuse SPs. In addition, extracellular expression of HspB2 was observed in CAA. Both Hsp27 and alphaB-crystallin were also observed in astrocytes associated with both SPs and CAA. Furthermore, none of the sHsps were observed in NFTs in AD brains. We conclude that specific sHsp species may be involved in the pathogenesis of either SPs or CAA in AD.

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Section: Discussionsupporting

confidence: 88%

Specific association of small heat shock proteins with the pathological hallmarks of Alzheimer's disease brains

Wilhelmus

Otte-Höller²,

Wesseling³

et al. 2006

Neuropathology Appl Neurobio

202

157

View full text Add to dashboard Cite

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“…Effects of Aβ on the vessel wall are particularly described for Aβ 1‐40 , whereas Aβ 1‐42 is mainly involved in senile plaque formation 14, 28. Because of the strong correlation between Aβ 1‐40 and Aβ 1‐42 plasma levels, we could not assess the individual effects of Aβ 1‐40 conditional on Aβ 1‐42 and vice versa.…”

Section: Discussionmentioning

confidence: 99%

Plasma amyloid β, apolipoprotein E, lacunar infarcts, and white matter lesions

Dijk¹,

Prins²,

Vermeer³

et al. 2004

Annals of Neurology

112

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Lacunar brain infarcts and cerebral white matter lesions are frequently observed on magnetic resonance imaging scans in elderly subjects. These lesions are also frequent in patient with cerebral amyloid angiopathy. We examined whether plasma amyloid beta peptide (Abeta) levels are associated with lacunar infarcts and white matter lesions in the general population, and whether the apolipoprotein E (APOE) genotype modifies these associations. We studied 1,077 participants within the population-based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia. Cross-sectional associations were analyzed by regression models with adjustments for age, sex, creatinine levels, and hypertension. In APOE epsilon4 carriers, plasma Abeta levels were positively associated with lacunar infarcts and white matter lesions, whereas in noncarriers no associations were observed. Per standard deviation increase in Abeta(1-40) and Abeta(1-42) levels the odds ratios for lacunar infarcts were 1.72 (95% confidence interval [CI] = 1.22-2.43) and 1.93 (95% CI = 1.31-2.85), the periventricular white matter lesion grade increased by 0.32 (95% CI = 0.08-0.57) and 0.29 (95% CI = 0.00-0.57), and the subcortical white matter lesion volume increased by 0.48 ml (95% CI = 0.04-0.91) and 0.24 ml (95% CI = -0.27-0.75). Higher Abeta levels are associated with more lacunar infarcts and white matter lesions in elderly subjects who carry an APOE epsilon4 allele.

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“…It has been demonstrated that CAA-affected vessels, unlike senile plaques, contain significant Aβ40 in addition to Aβ42, 49 which is abundantly found in senile plaques. This specific pattern of Aβ40/42 deposition in CAA is reflected by decreased levels of both Aβ40 and Aβ42 peptides in CSF obtained from patients with CAA, diagnosed according to the Boston criteria, 50 a finding replicated by other groups.…”

Section: Biomarkers Advances and Mechanistic Insightsmentioning

confidence: 99%

The increasing impact of cerebral amyloid angiopathy: essential new insights for clinical practice

Banerjee

Carare

Cordonnier

et al. 2017

J Neurol Neurosurg Psychiatry

183

137

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Cerebral amyloid angiopathy (CAA) has never been more relevant. The last 5 years have seen a rapid increase in publications and research in the field, with the development of new biomarkers for the disease, thanks to advances in MRI, amyloid positron emission tomography and cerebrospinal fluid biomarker analysis. The inadvertent development of CAA-like pathology in patients treated with amyloid-beta immunotherapy for Alzheimer’s disease has highlighted the importance of establishing how and why CAA develops; without this information, the use of these treatments may be unnecessarily restricted. Our understanding of the clinical and radiological spectrum of CAA has continued to evolve, and there are new insights into the independent impact that CAA has on cognition in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer’s and other dementias. While the association between CAA and lobar intracerebral haemorrhage (with its high recurrence risk) is now well recognised, a number of management dilemmas remain, particularly when considering the use of antithrombotics, anticoagulants and statins. The Boston criteria for CAA, in use in one form or another for the last 20 years, are now being reviewed to reflect these new wide-ranging clinical and radiological findings. This review aims to provide a 5-year update on these recent advances, as well as a look towards future directions for CAA research and clinical practice.

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Differences between the Pathogenesis of Senile Plaques and Congophilic Angiopathy in Alzheimer Disease

Abstract: M a r c e l M . V e r b e e k , P ie t E ik e l e n b o o m , a n d R o b e r t M . W . d e W a a l

Cited by 15 publications

References 33 publications

Specific association of small heat shock proteins with the pathological hallmarks of Alzheimer's disease brains

Specific association of small heat shock proteins with the pathological hallmarks of Alzheimer's disease brains

Plasma amyloid β, apolipoprotein E, lacunar infarcts, and white matter lesions

The increasing impact of cerebral amyloid angiopathy: essential new insights for clinical practice

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