ArticleJournal of neurology, neurosurgery, and psychiatry2022
Cerebellar atrophy and its implications on gait in cerebral amyloid angiopathy.
Article in Journal of neurology, neurosurgery, and psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Extent of Tau and Its Cognitive Implications in Patients With Cerebral Amyloid Angiopathy Without Cognitive Impairment.Neurology · 2026Article
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Apolipoprotein E Alleles and Motor Signs in Older Adults with Alzheimer's Dementia.International journal of molecular sciences · 2025Article
- Characterization of cerebellar amyloid-β deposits in Alzheimer disease.Journal of neuropathology and experimental neurology · 2024Article
- Subcortical volumes and cognition in CADASIL - A pilot study.Cerebral circulation - cognition and behavior · 2024Article
- Cerebral Amyloid Angiopathy: An Undeniable Small Vessel Disease.Journal of stroke · 2024Review
- Subcortical volumes in cerebral amyloid angiopathy compared with Alzheimer's disease and controls.Frontiers in neuroscience · 2023Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
objectiveRecent data suggest that cerebral amyloid angiopathy (CAA) causes haemorrhagic lesions in cerebellar cortex as well as subcortical cerebral atrophy. However, the potential effect of CAA on cerebellar tissue loss and its clinical implications have not been investigated.
methodsOur study included 70 non-demented patients with probable CAA, 70 age-matched healthy controls (HCs) and 70 age-matched patients with Alzheimer's disease (AD). The cerebellum was segmented into percent of cerebellar subcortical volume (pCbll-ScV) and percent of cerebellar cortical volume (pCbll-CV) represented as percent (p) of estimated total intracranial volume. We compared pCbll-ScV and pCbll-CV between patients with CAA, HCs and those with AD. Gait velocity (metres/second) was used to investigate gait function in patients with CAA.
resultsPatients with CAA had significantly lower pCbll-ScV compared with both HC (1.49±0.1 vs 1.73±0.2, p<0.001) and AD (1.49±0.1 vs 1.66±0.24, p<0.001) and lower pCbll-CV compared with HCs (6.03±0.5 vs 6.23±0.6, p=0.028). Diagnosis of CAA was independently associated with lower pCbll-ScV compared with HCs (p<0.001) and patients with AD (p<0.001) in separate linear regression models adjusted for age, sex and presence of hypertension. Lower pCbll-ScV was independently associated with worse gait velocity (β=0.736, 95% CI 0.28 to 1.19, p=0.002) in a stepwise linear regression analysis including pCbll-CV along with other relevant variables.
interpretationPatients with CAA show more subcortical cerebellar atrophy than HC or patients with AD and more cortical cerebellar atrophy than HCs. Reduced pCbll-ScV correlated with lower gait velocity in regression models including other relevant variables. Overall, this study suggests that CAA causes cerebellar injury, which might contribute to gait disturbance.
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