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Updated: May 22, 2025
Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Risk factors and clinical significance of neurodegenerative co-pathologies in symptomatic cerebral small vessel
Philipp Arndt1,2, Malte Pfister1, Valentina Perosa1,3
1Department of Neurology, Otto-Von-Guericke University, Leipziger Str. 44, 39120, Magdeburg, Germany.
Insights
Cerebral small vessel disease (CSVD) often co-occurs with neurodegenerative pathologies like Alzheimer's disease (AD) and non-AD changes, impacting cognitive function. Biomarker analysis in patients with deep perforator arteriopathy (DPA) or cerebral amyloid angiopathy (CAA) revealed these associations.
Area of Science:
- Neurology
- Neuroscience
- Biomarker Research
Background:
- Cerebral small vessel disease (CSVD) frequently coexists with neurodegenerative conditions.
- The interplay between CSVD and neurodegeneration, particularly in deep perforator arteriopathy (DPA) and cerebral amyloid angiopathy (CAA), requires further investigation.
- Understanding these relationships is crucial for diagnosing and managing cognitive decline.
Purpose of the Study:
- To determine the prevalence of neurodegenerative pathologies in patients with DPA or CAA.
- To identify risk factors associated with these coexisting conditions.
- To evaluate the impact of these pathologies on cognitive function using the ATN classification system.
Main Methods:
- A cross-sectional study involving 186 patients (median age 75) with probable CAA or DPA.
- Cerebrospinal fluid (CSF) biomarkers (Aβ42/40 ratio, p-tau, t-tau, NfL) and MRI for CSVD analysis were utilized.
- ATN profiles were correlated with clinical characteristics, MRI findings, and cognitive performance via multivariate regression.
Main Results:
- 30% of CSVD patients had normal biomarkers (A-T-N-).
- 33% showed Alzheimer's disease (AD) pathology continuum (A+T±N±), more prevalent in CAA (47%) than DPA (13%).
- 37% exhibited non-AD pathological changes (A-T±N+), more common in DPA (53%) than CAA (25%). Both AD and non-AD pathologies were linked to lower MMSE scores.
Conclusions:
- In vivo biomarker analysis confirms frequent co-occurrence of CSVD with neurodegenerative pathologies (AD and non-AD).
- Both AD pathology continuum and non-AD pathological changes significantly impact cognitive health, leading to lower MMSE scores.
- These findings highlight the detrimental effects of combined CSVD and neurodegeneration on cognitive function.
Background:
Cerebral small vessel disease (CSVD) often coexists with neurodegenerative pathologies, yet their role remains underexplored. This study aims to determine their prevalence, risk factors, and cognitive effects in patients with deep perforator arteriopathy (DPA) or cerebral amyloid angiopathy (CAA) using the biomarker-based ATN classification.
Methods:
In this cross-sectional study 186 patients (median age 75 years, 41% females, 111 with probable CAA, 75 with DPA) underwent MRI for analysis of CSVD severity and etiology, and lumbar puncture for analysis of cerebrospinal fluid amyloid-β 42/40 ratio, phosphorylated-tau, total-tau and neurofilament light. ATN profiles were related to clinical characteristics, MRI markers and cognitive performance in multivariate regression models.
Results:
Among CSVD patients, 30% had normal biomarkers (A-T-N-), 33% were within the AD pathology continuum (A + T ± N ± : 47% in CAA vs. 13% in DPA, p < .001), and 37% showed non-AD pathological changes (A-T ± N + : 53% in DPA vs. 25% in CAA, p < .001). The AD pathology continuum was associated with a severe lobar hemorrhagic phenotype and cognitive impairment, while non-AD pathological change was related to CSVD severity, history of stroke and similarly cognitive impairment. Both pathological ATN profiles were further related to lower MMSE scores (A + T ± N ± : B = - 3.3, p = .006; A-T ± N + : B = - 2.7, p = .021).
Conclusions:
Using biomarkers, this study confirms in vivo that CSVD frequently co-occurs with neurodegenerative pathologies, exerting detrimental effects on cognitive health.
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