Home > Publications Database > Alterations in MRI-visible perivascular spaces precede dementia diagnosis by 18 years in autosomal dominant Alzheimer's disease. > print

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024 7 _ |a 10.1002/alz.70588
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100 1 _ |a Kobeleva, Xenia
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245 _ _ |a Alterations in MRI-visible perivascular spaces precede dementia diagnosis by 18 years in autosomal dominant Alzheimer's disease.
260 _ _ |a Hoboken, NJ
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520 _ _ |a Perivascular space (PVS) alterations are traditionally linked to cardiovascular risk factors and aging, but may also play a direct role in Alzheimer's disease (AD). To reduce confounding from age-related comorbidities, we examined PVSs in autosomal dominant AD (ADAD).In this cross-sectional study of 96 non-demented individuals (62 mutation carriers), we quantified PVS count fraction and mean diameter in white matter and basal ganglia using automated magnetic resonance imaging analysis. Linear mixed models assessed group differences along the disease course, adjusting for cardiovascular risk factors.Compared to non-carriers, mutation carriers showed lower PVS count fraction in white matter and basal ganglia, and larger PVS diameter in basal ganglia and the temporal lobe. Changes were evident up to 18 years before expected dementia onset and followed trajectories similar to amyloid beta 42 and tau biomarkers.ADAD is associated with early PVS alterations, suggesting perivascular changes may be integral to primary AD pathology.Autosomal dominant Alzheimer's disease (ADAD) mutation carriers have reduced magnetic resonance imaging-visible perivascular space (PVS) count fraction in the white matter and basal ganglia. ADAD mutation carriers show enlarged PVS in the basal ganglia and temporal white matter. PVS alterations start 18 years before the estimated time of dementia diagnosis. The spatial localization of PVS changes overlaps with regions of amyloid beta (Aβ) accumulation. The temporal evolution of PVS alterations aligns with Aβ and tau changes in the cerebrospinal fluid.
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650 _ 7 |a Alzheimer's disease
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650 _ 7 |a autosomal dominant Alzheimer's disease
|2 Other
650 _ 7 |a cerebral small vessel disease
|2 Other
650 _ 7 |a dominantly inherited Alzheimer's disease
|2 Other
650 _ 7 |a magnetic resonance imaging
|2 Other
650 _ 7 |a perivascular spaces
|2 Other
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Magnetic Resonance Imaging
|2 MeSH
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Alzheimer Disease: diagnostic imaging
|2 MeSH
650 _ 2 |a Cross-Sectional Studies
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a White Matter: diagnostic imaging
|2 MeSH
650 _ 2 |a White Matter: pathology
|2 MeSH
650 _ 2 |a Glymphatic System: diagnostic imaging
|2 MeSH
650 _ 2 |a Glymphatic System: pathology
|2 MeSH
650 _ 2 |a Basal Ganglia: pathology
|2 MeSH
650 _ 2 |a Basal Ganglia: diagnostic imaging
|2 MeSH
650 _ 2 |a Mutation: genetics
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: cerebrospinal fluid
|2 MeSH
650 _ 2 |a tau Proteins: cerebrospinal fluid
|2 MeSH
650 _ 2 |a Disease Progression
|2 MeSH
700 1 _ |a Rowe, Bryan
|b 1
700 1 _ |a Choupan, Jeiran
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700 1 _ |a Ringman, John M
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700 1 _ |a Barisano, Giuseppe
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700 1 _ |a Leone, Riccardo
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773 _ _ |a 10.1002/alz.70588
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