Asset Details
Do you wish to reserve the book?
Associations between misfolded alpha‐synuclein aggregates and Alzheimer's disease pathology in vivo
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Associations between misfolded alpha‐synuclein aggregates and Alzheimer's disease pathology in vivo
Do you wish to request the book?
Associations between misfolded alpha‐synuclein aggregates and Alzheimer's disease pathology in vivo
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Associations between misfolded alpha‐synuclein aggregates and Alzheimer's disease pathology in vivo
2024
Overview
INTRODUCTION We examined the relations of misfolded alpha synuclein (α‐synuclein) with Alzheimer's disease (AD) biomarkers in two large independent cohorts. METHODS We included Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably Two (BioFINDER‐2) and Alzheimer's Disease Neuroimaging Initiative (ADNI) participants (n = 2315, cognitively unimpaired, mild cognitive impairment, AD dementia) who had cross‐sectional cerebrospinal fluid (CSF) α‐synuclein measurement from seed‐amplification assay as well as cross‐sectional and longitudinal amyloid beta (Aβ) and tau levels (measured in CSF and/or by positron emission tomography). All analyses were adjusted for age, sex, and cognitive status. RESULTS Across cohorts, the main biomarker associated with α‐synuclein positivity at baseline was higher levels of Aβ pathology (all p values ≤ 0.02), but not tau. Looking at longitudinal measures of AD biomarkers, α‐synuclein –positive participants had a statistically significant faster increase of Aβ load, although of modest magnitude (1.11 Centiloid/year, p = 0.02), compared to α‐synuclein –negative participants in BioFINDER‐2 but not in ADNI. DISCUSSION We showed associations between concurrent misfolded α‐synuclein and Aβ levels, providing in vivo evidence of links between these two molecular disease pathways in humans. Highlights: Amyloid beta (Aβ), but not tau, was associated with alpha‐synuclein (α‐synuclein) positivity. Such association was consistent across two cohorts, beyond the effect of age, sex, and cognitive status. α‐synuclein–positive participants had a small, statistically significant faster increase in Aβ positron emission tomography levels in one of the two cohorts.
Publisher
John Wiley and Sons Inc
Subject
/ alpha-Synuclein - cerebrospinal fluid
/ alpha-Synuclein - metabolism
/ Alzheimer Disease - cerebrospinal fluid
/ Alzheimer Disease - diagnostic imaging
/ Alzheimer Disease - metabolism
/ Alzheimer Disease - pathology
/ Amyloid beta-Peptides - cerebrospinal fluid
/ Amyloid beta-Peptides - metabolism
/ Biomarkers - cerebrospinal fluid
/ Cognitive Dysfunction - cerebrospinal fluid
/ Cognitive Dysfunction - metabolism
/ Female
/ Humans
/ Male
/ Medicinska och farmaceutiska grundvetenskaper
/ Positron-Emission Tomography
/ tau
