Cerebral microbleeds topography and cerebrospinal fluid biomarkers in cognitive impairment

Shams, Sara; Granberg, Tobias; Martola, Juha; Charidimou, Andreas; Li, Xiaozhen; Shams, Mana; Fereshtehnejad, Seyed‐Mohammad; Cavallin, Lena; Aspelin, Peter; Wiberg-Kristoffersen, Maria; Wahlund, Lars‐Olof

doi:10.1177/0271678x16649401

Cited by 26 publications

(16 citation statements)

References 39 publications

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“…4,18,24,25 Non-lobar microbleeds were not associated with change in MMSE score (P < 0.001), as demonstrated in previous studies. 4,26 One of the limitations of our study is that it lacked a comparison between T2* GRE sequences and SWI sequences in the detection of CMBs.…”

Section: Discussionsupporting

confidence: 76%

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Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer’s disease patients: A neuroimaging biomarker of the disease

et al. 2017

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Purpose: The objective of this study was to correlate the presence and distribution of cerebral microbleeds in Alzheimer's disease patients with cerebrospinal fluid biomarkers (amyloid-beta and phosphorylated tau 181 protein levels) and cognitive decline by using susceptibility-weighted imaging magnetic resonance sequences at 1.5 T. Material and methods: Fifty-four consecutive Alzheimer's disease patients underwent brain magnetic resonance imaging at 1.5 T to assess the presence and distribution of cerebral microbleeds on susceptibility-weighted imaging images. The images were analyzed in consensus by two neuroradiologists, each with at least 10 years' experience. Dementia severity was assessed with the Mini-Mental State Examination score. A multiple regression analysis was performed to assess the associations between the number and location of cerebral microbleed lesions with the age, sex, duration of the disease, cerebrospinal fluid amyloid-beta and phosphorylated tau 181 protein levels, and cognitive functions. Results: A total of 296 microbleeds were observed in 54 patients; 38 patients (70.4%) had lobar distribution, 13 patients (24.1%) had non-lobar distribution, and the remaining three patients (5.6%) had mixed distribution, demonstrating that Alzheimer's disease patients present mainly a lobar distribution of cerebral microbleeds. The age and the duration of the disease were correlated with the number of lobar cerebral microbleeds (P < 0.001). Cerebrospinal fluid amyloid-beta, phosphorylated tau 181 protein levels, and cognitive decline were correlated with the number of lobar cerebral microbleeds in Alzheimer's disease patients (P < 0.001). Conclusion: Lobar distribution of cerebral microbleeds is associated with Alzheimer's disease and the number of lobar cerebral microbleeds directly correlates with cerebrospinal fluid amyloid-beta and phosphorylated tau 181 protein levels and with the cognitive decline of Alzheimer's disease patients.

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Section: Discussionsupporting

confidence: 76%

“…17,18 In particular, of the 54 AD patients reviewed, 38 (70.4%) had a lobar distribution of the microbleeds, 13 (24.1%) had a non-lobar distribution and the remaining three (5.6%) had a mixed distribution (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer’s disease patients: A neuroimaging biomarker of the disease

et al. 2017

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“…APOE genotyping, through polymerase chain reaction, was performed for a subset of patients (n=520) on coded genomic DNA samples. CSF samples were obtained by lumbar puncture and were available for 1039 patients, and the procedure of analysis has been described elsewhere . CSF was analyzed for amyloid β 42 (Innotest β‐Amyloid(1‐42)), total tau (T‐tau) (Innotest hTau‐Ag), and tau phosphorylated at threonine 181 ( P ‐tau) (Innotest Phospho‐tau(181P); Innogenetics, Ghent, Belgium).…”

Section: Methodsmentioning

confidence: 99%

Topography and Determinants of Magnetic Resonance Imaging (MRI)‐Visible Perivascular Spaces in a Large Memory Clinic Cohort

Shams

Martola

Charidimou

et al. 2017

JAHA

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BackgroundMagnetic resonance imaging‐visible perivascular spaces (PVS) are related to interstitial fluid clearance pathways (including amyloid‐β) in the brain and are suggested to be a marker of cerebral small vessel disease. We investigated the role, topography, and possible implications of PVS in cognitive impairment.Methods and ResultsA total of 1504 patients undergoing memory clinic investigation and an associated brain magnetic resonance imaging scan were included in this cross‐sectional study. Magnetic resonance images were assessed for markers of small vessel disease. Additionally, 1039 patients had cerebrospinal fluid analysis of amyloid‐β 42, total tau (T‐tau), and phosphorylated tau (P‐tau); 520 patients had apoE genotyping done. Results were analyzed with generalized linear models. A total of 289 (19%; 95% confidence interval, 17–21) had a high‐grade PVS in the centrum semiovale (CSO) and 65 (4%; 95% confidence interval: 3%–5%) in the basal ganglia (BG). Centrum semiovale– and BG‐PVS were both associated with high age (P<0.001), hypertension (P<0.001), probable cerebral amyloid angiopathy (P<0.05), moderate‐to‐severe white matter hyperintensities (P<0.001), cortical superficial siderosis (P<0.001), cerebral microbleeds (P<0.001), and PVS. centrum semiovale–PVS was separately associated with strictly lobar cerebral microbleeds (P=0.057). BG‐PVS was associated with strictly deep cerebral microbleeds (P<0.001), lacunes (P<0.001), and vascular dementia (P=0.04). BG‐PVS showed a tendency to be associated with high cerebrospinal fluid tau (B=0.002, P=0.04) in the whole cohort and in Alzheimer's disease (B=0.005; P=0.02). No other associations with cerebrospinal fluid or the apoE e4 allele was observed.ConclusionsCentrum semiovale–PVS and BG‐PVS have different underlying etiology, being associated with cerebral amyloid angiopathy and hypertensive vasculopathy, respectively, although a significant overlap between these pathologies is likely to exist.

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“…The majority of those studies found a relationship between cerebral Aβ load and CSVD marker burden (e.g. ), while only few failed (e.g. ).…”

Section: Interaction Between Dpa and Caa – Pathophysiological Considementioning

confidence: 99%

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

Schreiber

Wilisch‐Neumann

Schreiber

et al. 2019

Neuropathology Appl Neurobio

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Invited Review: The spectrum of age-related small vessel diseases: potential overlap and interactions of amyloid and nonamyloid vasculopathiesDeep perforator arteriopathy (DPA) and cerebral amyloid angiopathy (CAA) are the commonest known cerebral small vessel diseases (CSVD), which cause ischaemic stroke, intracebral haemorrhage (ICH) and vascular cognitive impairment (VCI). While thus far mainly considered as separate entities, we here propose that DPA and CAA share similarities, overlap and interact, so that 'pure' DPA or CAA are extremes along a continuum of age-related small vessel pathologies. We suggest blood-brain barrier (BBB) breakdown, endothelial damage and impaired perivascular b-amyloid (Ab) drainage are hallmark common mechanisms connecting DPA and CAA. We also suggest a need for new biomarkers (e.g. high-resolution imaging) to deepen understanding of the complex relationships between DPA and CAA.

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Cerebral microbleeds topography and cerebrospinal fluid biomarkers in cognitive impairment

Cited by 26 publications

References 39 publications

Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer’s disease patients: A neuroimaging biomarker of the disease

Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer’s disease patients: A neuroimaging biomarker of the disease

Topography and Determinants of Magnetic Resonance Imaging (MRI)‐Visible Perivascular Spaces in a Large Memory Clinic Cohort

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

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