Khazar Ahmadi, Sweden
Lund University Department of Clinical SciencesAuthor Of 2 Presentations
LIVE DISCUSSION
ALTERED CEREBRAL BLOOD PERFUSION IN ALZHEIMER’S DISEASE SPECTRUM AND ITS ASSOCIATION WITH AMYLOID-BETA AND TAU PATHOLOGY
Abstract
Aims
A large body of research has shown cerebral blood hypoperfusion across the Alzheimer’s disease (AD) continuum. However, the relationship between the primary AD pathologies and cerebral blood flow (CBF) remains unclear. Here, we examined the link between amyloid-beta (Aβ) and tau with CBF.
Methods
Baseline CBF was measured by arterial spin labeling at a 3T MRI scanner in 94 Aβ- cognitively unimpaired, 43 Aβ+ cognitively unimpaired, and 119 Aβ+ cognitively impaired participants i.e. those with mild cognitive impairment (MCI) or AD dementia. Aβ and tau burden was measured using [18F] flutemetamol and [18F] RO948 positron emission tomography (PET), respectively. Additionally, cerebrospinal fluid (CSF) was analyzed for Aβ42 and Aβ40. Voxel-wise and linear regression analyses were used to assess the interrelation between CBF with Aβ and tau load.
Results
CBF was not associated with amyloid PET or CSF Aβ42/40 in cognitively unimpaired individuals. However, tau PET was inversely related to CBF in lateral temporal, parietal and superior occipital cortices in individuals on the AD continuum i.e. in Aβ+ individuals. Event-based modeling suggested that the observed CBF alterations occurred after neocortical Aβ pathology, temporal tau pathology, and memory deficits, but before widespread neocortical tau pathology.
Conclusions
These findings provide in vivo evidence for an association between tau aggregation and CBF reduction in the AD spectrum and indicate that CBF changes after the occurrence of tau pathology in temporal areas.
Presenter of 2 Presentations
ALTERED CEREBRAL BLOOD PERFUSION IN ALZHEIMER’S DISEASE SPECTRUM AND ITS ASSOCIATION WITH AMYLOID-BETA AND TAU PATHOLOGY
Abstract
Aims
A large body of research has shown cerebral blood hypoperfusion across the Alzheimer’s disease (AD) continuum. However, the relationship between the primary AD pathologies and cerebral blood flow (CBF) remains unclear. Here, we examined the link between amyloid-beta (Aβ) and tau with CBF.
Methods
Baseline CBF was measured by arterial spin labeling at a 3T MRI scanner in 94 Aβ- cognitively unimpaired, 43 Aβ+ cognitively unimpaired, and 119 Aβ+ cognitively impaired participants i.e. those with mild cognitive impairment (MCI) or AD dementia. Aβ and tau burden was measured using [18F] flutemetamol and [18F] RO948 positron emission tomography (PET), respectively. Additionally, cerebrospinal fluid (CSF) was analyzed for Aβ42 and Aβ40. Voxel-wise and linear regression analyses were used to assess the interrelation between CBF with Aβ and tau load.
Results
CBF was not associated with amyloid PET or CSF Aβ42/40 in cognitively unimpaired individuals. However, tau PET was inversely related to CBF in lateral temporal, parietal and superior occipital cortices in individuals on the AD continuum i.e. in Aβ+ individuals. Event-based modeling suggested that the observed CBF alterations occurred after neocortical Aβ pathology, temporal tau pathology, and memory deficits, but before widespread neocortical tau pathology.
Conclusions
These findings provide in vivo evidence for an association between tau aggregation and CBF reduction in the AD spectrum and indicate that CBF changes after the occurrence of tau pathology in temporal areas.
LIVE DISCUSSION