Dementia incidence and predictors in cerebral amyloid angiopathy patients without intracerebral hemorrhage

Abstract

Cerebral amyloid angiopathy (CAA) is a common cause of cognitive impairment in older individuals. This study aimed to investigate predictors of dementia in CAA patients without intracerebral hemorrhage (ICH). A total of 158 non-demented patients from the Stroke Service or the Memory Clinic who met the modified Boston Criteria for probable CAA were included. At baseline, neuroimaging markers, including lobar microbleeds (cerebral microbleeds (CMBs)), white matter hyperintensities (WMH), cortical superficial siderosis (cSS), magnetic resonance imaging (MRI)-visible centrum semiovale perivascular spaces (CSO-PVS), lacunes, and medial temporal atrophy (MTA) were assessed. The overall burden of small vessel disease (SVD) for CAA was calculated by a cumulative score based on CMB number, WMH severity, cSS presence and extent and CSO-PVS severity. The estimated cumulative dementia incidence at 1 year was 14% (95% confidence interval (CI): 5%-23%), and 5 years 73% (95% CI: 55%, 84%). Age (hazard ratio (HR) 1.05 per year, 95% CI: 1.01-1.08, p = 0.007), presence of MCI status (HR 3.40, 95% CI: 1.97-6.92, p < 0.001), MTA (HR 1.71 per point, 95% CI: 1.26-2.32, p = 0.001), and SVD score (HR 1.23 per point, 95% CI: 1.20-1.48, p = 0.030) at baseline were independent predictors for dementia conversion in these patients. Cognitive deterioration of CAA patients appears attributable to cumulative changes, from both vasculopathic and neurodegenerative lesions.

Enlarged Perivascular Spaces and Dementia: A Systematic Review

“…Thirteen articles met the aforementioned criteria ( Fig. 1) [16][17][18][19][20][21][22][23][24][25][26][27][28]. Three studies analyzed longitudinal data [16,17,19] and ten were cross-sectional studies [18,[20][21][22][23][24][25][26][27][28].…”

“…The follow-up time ranged from 2.3 years (median) to 5.2 years (mean). Two studies reported the number of cases of all-cause dementia [17,19], whereas one study specified the subtypes, i.e., AD and VaD [16]. Two studies examined the general population and one study examined subjects with probable CAA.…”

“…Furthermore, different definitions were used to determine 'severe' burden of ePVS which were either based on categories (derived from counts data), size, or weightage of PVS. The following definitions were encountered: presence of >20 ePVS [19,23,27], presence of >10 ePVS [17,18,28], presence of ePVS > 2 mm [20], presence of ePVS > 3 mm [16], and weighting in the location of ePVS [21,22]. Three studies used continuous measures for ePVS [22,24,26].…”

“…Besides one paper [24], all studies performed statistical analysis on the association between ePVS and dementia diagnosis within the context of multivariate models. Variables were included in statistical analysis on the basis of biology of the disease, as well as by significance testing, i.e., selection of only those variables with p-values less than 0.05 or 0.1 in preliminary analysis [19,23]. Commonly included variables were age, gender, other MRI-markers, cardiovascular risk factors, education, and cognitive scores.…”

Invited Review: The spectrum of age‐related small vessel diseases: potential overlap and interactions of amyloid and nonamyloid vasculopathies

“…Both DPA and CAA are the major sources of VCI and vascular dementia , with a cumulative dementia incidence of around 70% after 5 years for CAA patients . Around one of three of the DPA and CAA subjects seem to reveal VCI, with disturbed executive function and reduced processing speed as well as CAA‐related visuoperceptual impairment being the most consistent findings .…”