Related Experiment Video
Updated: May 31, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
Published on: March 7, 2019
Cerebral microhemorrhage and brain β-amyloid in aging and Alzheimer disease
P A Yates1, R Sirisriro, V L Villemagne
1Department of Nuclear Medicine and Centre for PET, Austin Health, 145 Studley Road, Heidelberg, Victoria 3084, Australia. paul.yates@austin.org.au
Objectives:
Incidental cerebral microhemorrhage (MH) is frequently found in older individuals scanned with susceptibility-weighted MRI (SWI) or gradient-recalled echo MRI. MH have been linked with β-amyloid (Aβ) deposition using (11)C-Pittsburgh compound B (PiB) PET in Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA). We hypothesized that Aβ deposition in asymptomatic elderly individuals is associated with lobar MH (LMH).
Methods:
This was a cross-sectional study of 84 elderly healthy controls (HC), 28 subjects with mild cognitive impairment (MCI), and 26 subjects with probable AD who underwent 3-T SWI and (11)C-PiB PET. (11)C-PiB cortical binding was quantified normalized to cerebellar cortex (standardized uptake value ratio [SUVR]) and scans classified as positive (PiB+) or negative (PiB-) by visual inspection. MH were manually counted and categorized by region and as lobar or nonlobar.
Results:
LMH were present in 30.8% of AD, 35.7% of MCI, and 19.1% of HC. The prevalence of LMH among PiB+ subjects was similar, regardless of clinical classification (AD 30.8%, MCI 38.9%, HC 41.4%, p > 0.7). HC with LMH had significantly higher mean neocortical SUVR (1.7 ± 0.5) than HC without LMH (1.3 ± 0.3, p ± 0.01). In HC, there was a positive correlation between number of LMH and SUVR, and between LMH and age. In HC, PiB+ (odds ratio [OR] 7.3, 95% confidence interval [CI] 1.6-33.7, p = 0.01) and age (OR 1.2, 95% CI 1.03-1.3, p = 0.02) both independently predicted the occurrence of LMH using logistic regression.
Conclusion:
Asymptomatic Aβ deposition in older adults is strongly associated with LMH.
Insights
Asymptomatic beta-amyloid (Aβ) deposition in older adults is linked to lobar cerebral microhemorrhages (LMH). This finding suggests Aβ may play a role in microhemorrhage development even before cognitive decline.
Area of Science:
- Neuroimaging
- Neuropathology
- Geriatric Medicine
Background:
- Cerebral microhemorrhages (MH) are common in older adults, often detected via MRI.
- MH have been associated with beta-amyloid (Aβ) deposition in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
Purpose of the Study:
- To investigate the association between Aβ deposition and lobar MH (LMH) in asymptomatic elderly individuals.
- To determine if Aβ deposition predicts LMH in healthy older adults.
Main Methods:
- Cross-sectional study involving healthy controls (HC), mild cognitive impairment (MCI), and probable AD subjects.
- Utilized 3-Tesla susceptibility-weighted MRI (SWI) for MH detection and (11)C-Pittsburgh compound B (PiB) PET for Aβ deposition quantification.
- MH were manually counted and categorized; Aβ cortical binding was quantified as standardized uptake value ratio (SUVR).
Main Results:
- Lobar MH (LMH) prevalence was observed across all groups, including HC.
- PiB-positive (PiB+) subjects showed similar LMH prevalence regardless of clinical status.
- In HC, LMH presence correlated positively with neocortical Aβ deposition (SUVR) and age.
- PiB+ status and age independently predicted LMH occurrence in HC.
Conclusions:
- Asymptomatic Aβ deposition in older adults is strongly associated with LMH.
- This suggests a potential role for Aβ in the development of microhemorrhages, even in the absence of clinical symptoms.
Related Concept Videos
Alzheimer Disease ll: Pathophysiology
Alzheimer Disease l: Introduction
Dementia l: Introduction
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Hemorrhagic Stroke l: Introduction
Cerebral Edema ll: Pathophysiology

