O1-01-03: Alzheimer disease pathology influences the impact of cerebral amyloid angiopathy on cognitive decline

2006 ◽  
Vol 2 ◽  
pp. S8-S8
Author(s):  
Magdalena Quass ◽  
Johannes Attems ◽  
Kurt A. Jellinger ◽  
Felix Lintner
Keyword(s):  
Alzheimer Disease ◽  
Cognitive Decline ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
The Impact ◽  
Alzheimer Disease Pathology

scholarly journals Cerebral Atherosclerosis Is Associated With Cystic Infarcts and Microinfarcts but Not Alzheimer Pathologic Changes

Stroke ◽  
2013 ◽  
Vol 44 (10) ◽  
pp. 2835-2841 ◽  
Author(s):  
Ling Zheng ◽  
Harry V. Vinters ◽  
Wendy J. Mack ◽  
Chris Zarow ◽  
William G. Ellis ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Braak Stage ◽  
Autopsy Study ◽  
Plaque Score ◽  
Lacunar Infarcts ◽  
Cerebral Atherosclerosis ◽  
Cerebral Amyloid ◽  
Alzheimer Disease Pathology

Background and Purpose— Some studies have reported associations between intracranial atherosclerosis and Alzheimer disease pathology. We aimed to correlate severity of cerebral atherosclerosis, arteriolosclerosis, and cerebral amyloid angiopathy with neurofibrillary tangles, neuritic plaques, and cerebral infarcts. Methods— This autopsy study (n=163) was drawn from a longitudinal study of subcortical ischemic vascular disease, Alzheimer disease, and normal aging. Multivariable logistic regression models were used to test associations among the 3 forms of cerebrovascular disease and the presence of ischemic and neurodegenerative brain lesions. Apolipoprotein E genotype was included as a covariate in these multivariable models. Results— Cerebral atherosclerosis was positively associated with microinfarcts (odds ratio [OR], 2.3; 95% confidence interval [CI], 1.2–4.4) and cystic infarcts (OR, 2.0; 95% CI, 1.0–4.2) but not Alzheimer disease pathology. Arteriolosclerosis showed a positive correlation with lacunar infarcts (OR, 2.0; 95% CI, 1.0–4.2) but not Alzheimer disease pathology. Cerebral amyloid angiopathy was inversely associated with lacunar infarcts (OR, 0.6; 95% CI, 0.41–1.1), but positively associated with Braak and Braak stage (OR, 1.5; 95% CI, 1.1–2.1) and Consortium to Establish a Registry for Alzheimer Disease plaque score (OR, 1.5; 95% CI, 1.1–2.2). Conclusions— Microinfarcts, which have been correlated with severity of cognitive impairment, were most strongly associated with atherosclerosis. Possible pathogenetic mechanisms include artery-to-artery emboli, especially microemboli that may include atheroemboli or platelet-fibrin emboli. Arteriolosclerosis was positively, whereas cerebral amyloid angiopathy was negatively correlated with lacunar infarcts, which might prove helpful in clinical differentiation of arteriolosclerotic from cerebral amyloid angiopathy–related vascular brain injury.

scholarly journals PSEN1 Compound Heterozygous Mutations Associated with Cerebral Amyloid Angiopathy and Cognitive Decline Phenotype

2021 ◽  
Vol 22 (8) ◽  
pp. 3870
Author(s):  
Ilaria Palmieri ◽  
Marialuisa Valente ◽  
Lisa Maria Farina ◽  
Simone Gana ◽  
Brigida Minafra ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Cognitive Decline ◽  
Cerebral Amyloid Angiopathy ◽  
Presenilin 1 ◽  
Compound Heterozygous ◽  
Amyloid Angiopathy ◽  
First Case ◽  
Cerebral Amyloid ◽  
Compound Heterozygous Mutations ◽  
The Impact

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by the deposition of amyloid beta-peptide (Aβ) aggregates. Aβ aggregates lead to vessel rupture and intracerebral hemorrhages, detected by magnetic resonance imaging (MRI). Presenile CAA is usually genetically determined by mutations in the amyloid precursor protein (APP) gene. However, mutations after codon 200 in the presenilin 1 (PSEN1) gene have been reported to facilitate CAA onset. Here, we analyzed the genetic bases in a patient of 55 years old affected by CAA and cognitive decline. DNA was isolated and genetic analysis was performed by Next-Generation Sequencing (NGS). RNA was extracted and retro-transcribed to perform segregation analysis by TOPO-TA cloning. WB analysis was carried out to check the impact of the mutations on protein. Two compound heterozygous mutations in PSEN1 exon 10, such as a novel stop-gain mutation (c.1070C > G) and a pathogenic splice variant (c.1129A > T), were found by NGS. Both mutations altered the presenilin 1 protein, truncating its C-terminal portion. This is the first case of CAA and cognitive decline caused by two compound mutations in PSEN1. With this report, we suggest extending the genetic analysis to PSEN1 when cerebral microbleeds are observed by MRI investigation in a patient affected by presenile cognitive decline.

scholarly journals Successful electroconvulsive therapy for depression in a man with cerebral amyloid angiopathy

2021 ◽  
Vol 14 (2) ◽  
pp. e238922
Author(s):  
Geert Schurgers ◽  
Baer M G Arts ◽  
Alida A Postma ◽  
Anna de Kort
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Electroconvulsive Therapy ◽  
Severe Depression ◽  
Amyloid Angiopathy ◽  
Amyloid Beta Protein ◽  
Cerebral Blood Vessels ◽  
Safety Measures ◽  
Aβ Clearance ◽  
Cerebral Amyloid ◽  
The Impact

Cerebral amyloid angiopathy (CAA) is a condition characterised by accumulation of amyloid beta protein (Aβ) in the wall of cerebral blood vessels which increases the risk of intracranial haemorrhage and contributes to cognitive impairment. We describe the case of a man around the age of 70 with ‘probable’ CAA according to the modified Boston criteria and severe depression whose depression was treated successfully with electroconvulsive therapy (ECT). To the best of our knowledge, there are no earlier published reports of ECT in a patient with CAA. We briefly discuss possible safety measures for these patients, the impact of ECT on cognition in CAA and a possible influence of ECT on Aβ clearance.

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