Cerebrovascular and Neurodegenerative Pathologies in Long-Term Stable Mild Cognitive Impairment

2021 ◽  
pp. 1-15
Author(s):  
Manu J. Sharma ◽  
Brandy L. Callahan
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cerebral Amyloid Angiopathy ◽  
Neurofibrillary Tangles ◽  
Small Vessel Disease ◽  
Significant Proportion ◽  
Amyloid Angiopathy ◽  
Prodromal Phase ◽  
Cerebral Amyloid

Background: Mild cognitive impairment (MCI) is considered by some to be a prodromal phase of a progressive disease (i.e., neurodegeneration) resulting in dementia; however, a substantial portion of individuals (ranging from 5–30%) remain cognitively stable over the long term (sMCI). The etiology of sMCI is unclear but may be linked to cerebrovascular disease (CVD), as evidence from longitudinal studies suggest a significant proportion of individuals with vasculopathy remain stable over time. Objective: To quantify the presence of neurodegenerative and vascular pathologies in individuals with long-term (>5-year) sMCI, in a preliminary test of the hypothesis that CVD may be a contributor to non-degenerative cognitive impairment. We expect frequent vasculopathy at autopsy in sMCI relative to neurodegenerative disease, and relative to individuals who convert to dementia. Methods: In this retrospective study, using data from the National Alzheimer’s Coordinating Center, individuals with sMCI (n = 28) were compared to those with MCI who declined over a 5 to 9-year period (dMCI; n = 139) on measures of neurodegenerative pathology (i.e., Aβ plaques, neurofibrillary tangles, TDP-43, and cerebral amyloid angiopathy) and CVD (infarcts, lacunes, microinfarcts, hemorrhages, and microbleeds). Results: Alzheimer’s disease pathology (Aβ plaques, neurofibrillary tangles, and cerebral amyloid angiopathy) was significantly higher in the dMCI group than the sMCI group. Microinfarcts were the only vasculopathy associated with group membership; these were more frequent in sMCI. Conclusion: The most frequent neuropathology in this sample of long-term sMCI was microinfarcts, tentatively suggesting that silent small vessel disease may characterize non-worsening cognitive impairment.

scholarly journals Cerebrovascular reactivity in cerebral amyloid angiopathy, Alzheimer disease, and mild cognitive impairment

Neurology ◽  
2020 ◽  
Vol 95 (10) ◽  
pp. e1333-e1340 ◽  
Author(s):  
Aaron R. Switzer ◽  
Ikreet Cheema ◽  
Cheryl R. McCreary ◽  
Angela Zwiers ◽  
Anna Charlton ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Alzheimer Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Response Amplitude ◽  
Cerebrovascular Reactivity ◽  
White Matter Hyperintensity ◽  
Amyloid Angiopathy ◽  
Bold Response ◽  
Cerebral Amyloid

ObjectiveTo assess cerebrovascular reactivity in response to a visual task in participants with cerebral amyloid angiopathy (CAA), Alzheimer disease (AD), and mild cognitive impairment (MCI) using fMRI.MethodsThis prospective cohort study included 40 patients with CAA, 22 with AD, 27 with MCI, and 25 healthy controls. Each participant underwent a visual fMRI task using a contrast-reversing checkerboard stimulus. Visual evoked potentials (VEPs) were used to compare visual cortex neuronal activity in 83 participants. General linear models using least-squares means, adjusted for multiple comparisons with the Tukey test, were used to estimate mean blood oxygen level–dependent (BOLD) signal change during the task and VEP differences between groups.ResultsAfter adjustment for age and hypertension, estimated mean BOLD response amplitude was as follows: CAA 1.88% (95% confidence interval [CI] 1.60%–2.15%), AD 2.26% (1.91%–2.61%), MCI 2.15% (1.84%–2.46%), and control 2.65% (2.29%–3.00%). Only patients with CAA differed from controls (p = 0.01). In the subset with VEPs, group was not associated with prolonged latencies or lower amplitudes. Lower BOLD amplitude response was associated with higher white matter hyperintensity (WMH) volumes in CAA (for each 0.1% lower BOLD response amplitude, the WMH volume was 9.2% higher, 95% CI 6.0%–12.4%) but not other groups (p = 0.002 for interaction) when controlling for age and hypertension.ConclusionsMean visual BOLD response amplitude was lowest in participants with CAA compared to controls, without differences in VEP latencies and amplitudes. This suggests that the impaired visual BOLD response is due to reduced vascular reactivity in CAA. In contrast to participants with CAA, the visual BOLD response amplitude did not differ between those with AD or MCI and controls.

Cerebral Amyloid Angiopathy Is Associated With Executive Dysfunction and Mild Cognitive Impairment

Stroke ◽  
2016 ◽  
Vol 47 (8) ◽  
pp. 2010-2016 ◽  
Author(s):  
Nevicia F. Case ◽  
Anna Charlton ◽  
Angela Zwiers ◽  
Saima Batool ◽  
Cheryl R. McCreary ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cerebral Amyloid Angiopathy ◽  
Executive Dysfunction ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals The Contribution of Vascular Pathology Toward Cognitive Impairment in Older Individuals with Intermediate Braak Stage Tau Pathology

2020 ◽  
Vol 77 (3) ◽  
pp. 1005-1015 ◽  
Author(s):  
Andrew C. Robinson ◽  
Federico Roncaroli ◽  
Stephen Chew-Graham ◽  
Yvonne S. Davidson ◽  
James Minshull ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Vascular Pathology ◽  
Cognitively Impaired ◽  
Amyloid Angiopathy ◽  
Braak Stage ◽  
Age Related ◽  
Cerebral Amyloid

Background: The pathological features of Alzheimer’s disease (AD) are well described but little is known as to how both neurodegeneration and vascular changes might interact in causing cognitive impairment. Objective: The present study aims to investigate relationships between vascular and AD pathology in cognitively healthy and cognitively impaired individuals with a particular emphasis on those at intermediate Braak tau stages. Methods: We investigated the interplay between Braak tau stage and measures of vascular pathology as described by the vascular cognitive impairment neuropathology guidelines (VCING) in 185 brains from the Brains for Dementia Research programme and The University of Manchester Longitudinal Study of Cognition in Healthy Old Age. VCING asserts that at least one large (>10 mm) infarct, moderate/severe occipital leptomeningeal cerebral amyloid angiopathy, and moderate/severe arteriosclerosis in occipital white matter accurately predicts the contribution of cerebrovascular pathology to cognitive impairment. Results: We found that the extent of arteriosclerosis in the occipital white matter did not differ between cognitive groups at intermediate (III-IV) Braak stages whereas moderate/severe leptomeningeal occipital cerebral amyloid angiopathy was greater in cognitively impaired than normal individuals at Braak stage III-IV. This finding remained significant after controlling for effects of age, sex, CERAD score, Thal phase, presence/severity of primary age-related tauopathy, presence/severity of limbic-predominant age-related TDP43 encephalopathy and small vessel disease in basal ganglia. Conclusion: Interventions targeting cerebral amyloid angiopathy may contribute to delay the onset of cognitive impairment in individuals with intermediate Alzheimer’s type pathology.

scholarly journals 10-Year Follow-Up of a Patient with Cerebral Amyloid Angiopathy

2020 ◽  
Vol 12 (Suppl. 1) ◽  
pp. 202-206
Author(s):  
Min Kyoung Kang ◽  
Byung-Woo Yoon
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
The Elderly ◽  
Amyloid Angiopathy ◽  
Spontaneous Intracerebral Hemorrhage ◽  
Radiological Features ◽  
Magnetic Imaging ◽  
Long Term Follow Up ◽  
Cerebral Amyloid

We report the case of long-term follow-up of brain magnetic imaging of cerebral amyloid angiopathy. Cerebral amyloid angiopathy is often considered a major cause of spontaneous intracerebral hemorrhage in the elderly. This case illustrates the markedly progressive clinical and radiological features of the vasculopathic process in 10 years.

scholarly journals Cerebral amyloid angiopathy severity is linked to dilation of juxtacortical perivascular spaces

2015 ◽  
Vol 36 (3) ◽  
pp. 576-580 ◽  
Author(s):  
Susanne J van Veluw ◽  
Geert Jan Biessels ◽  
Willem H Bouvy ◽  
Wim GM Spliet ◽  
Jaco JM Zwanenburg ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Resonance Imaging ◽  
Centrum Semiovale ◽  
Tissue Sections ◽  
Cortical Areas ◽  
Cerebral Amyloid

Perivascular spaces are an emerging marker of small vessel disease. Perivascular spaces in the centrum semiovale have been associated with cerebral amyloid angiopathy. However, a direct topographical relationship between dilated perivascular spaces and cerebral amyloid angiopathy severity has not been established. We examined this association using post-mortem magnetic resonance imaging in five cases with evidence of cerebral amyloid angiopathy pathology. Juxtacortical perivascular spaces dilation was evaluated on T2 images and related to cerebral amyloid angiopathy severity in overlying cortical areas on 34 tissue sections stained for Amyloid β. Degree of perivascular spaces dilation was significantly associated with cerebral amyloid angiopathy severity (odds ratio = 3.3, 95% confidence interval 1.3–7.9, p = 0.011). Thus, dilated juxtacortical perivascular spaces are a promising neuroimaging marker of cerebral amyloid angiopathy severity.

Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is independent of plaques and neurofibrillary tangles

2001 ◽  
Vol 50 (6) ◽  
pp. 765-772 ◽  
Author(s):  
Remco Natté ◽  
Marion L. C. Maat-Schieman ◽  
Joost Haan ◽  
Marjolijn Bornebroek ◽  
Raymund A.C. Roos ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Neurofibrillary Tangles ◽  
Cerebral Hemorrhage ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Cerebral amyloid angiopathy: subtypes, treatment and role in cognitive impairment

2017 ◽  
Vol 264 (10) ◽  
pp. 2184-2186 ◽  
Author(s):  
D. McLauchlan ◽  
G. A. Malik ◽  
N. P. Robertson
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Index event of cerebral amyloid angiopathy (CAA) determines long-term prognosis and recurrent events (retrospective analysis and clinical follow-up)

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Andrea Wagner ◽  
Christiane Groetsch ◽  
Sibylle Wilfling ◽  
Karl-Michael Schebesch ◽  
Mustafa Kilic ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Recurrent Events ◽  
Clinical Presentation ◽  
Secondary Prophylaxis ◽  
Amyloid Angiopathy ◽  
Index Event ◽  
Asymptomatic Patients ◽  
Cerebral Amyloid

Abstract Background The modified Boston criteria (mBC) define the probability for the diagnosis of cerebral amyloid angiopathy (CAA). Its initial clinical presentation differs from asymptomatic cerebral microbleedings (cMBs), acute ischemic stroke (AIS), cortical hemosiderosis (cSS), to lobar ICH (lICH). Methods Retrospective analyses and clinical follow-ups of individuals with at least mBC “possible” CAA from 2005 to 2018. Results 149 patients were classified in subgroups due to the index event: lICH (n = 91), AIS (n = 32), > 3 cMBs only (n = 16) and cSS (n = 10). Patients in the lICH subgroup had a significantly higher percentage of single new lICHs compared to other groups, whereas patients in the AIS-group had a significantly higher percentage of multiple new AIS. cMBs as index event predisposed for AIS during follow up (p < 0.0016). Patients of the cMBs- or cSS-group showed significantly more TFNEs (transient focal-neurological episodes) and lower numbers of asymptomatic patients (for epilepsy and TFNEs) at the index event than patients with lICH or AIS (p < 0.0013). At long-term follow-up, the cMBs- and cSS-group were characterized by more TFNEs and fewer asymptomatic patients. Conclusions A new classification system of CAA should add subgroups according to the initial clinical presentation to the mBCs allowing individual prognosis, acute treatment and secondary prophylaxis.

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