Plasma tau predicts cerebral vulnerability in aging.
Age Factors
Aged
Aging
/ blood
Amyloid beta-Peptides
/ metabolism
Cerebral Cortex
/ diagnostic imaging
Cognition
Cognitive Aging
Cognitive Dysfunction
/ blood
Female
Glucose
/ metabolism
Humans
Magnetic Resonance Imaging
Male
Memory
Middle Aged
Neuropsychological Tests
Peptide Fragments
/ metabolism
Positron Emission Tomography Computed Tomography
Risk Factors
tau Proteins
/ blood
FDG-PET
aging
cerebral vulnerability
cortical thickness
plasma tau
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
04 11 2020
04 11 2020
Historique:
received:
13
06
2020
accepted:
25
08
2020
pubmed:
5
11
2020
medline:
24
4
2021
entrez:
4
11
2020
Statut:
ppublish
Résumé
Identifying cerebral vulnerability in late life may help prevent or slow the progression of aging-related chronic diseases. However, non-invasive biomarkers aimed at detecting subclinical cerebral changes in the elderly are lacking. Here, we have examined the potential of plasma total tau (t-tau) for identifying cerebral and cognitive deficits in normal elderly subjects. Patterns of cortical thickness and cortical glucose metabolism were used as outcomes of cerebral vulnerability. We found that increased plasma t-tau levels were associated with widespread reductions of cortical glucose uptake, thinning of the temporal lobe, and memory deficits. Importantly, tau-related reductions of glucose consumption in the orbitofrontal cortex emerged as a determining factor of the relationship between cortical thinning and memory loss. Together, these results support the view that plasma t-tau may serve to identify subclinical cerebral and cognitive deficits in normal aging, allowing detection of individuals at risk for developing aging-related neurodegenerative conditions.
Identifiants
pubmed: 33147571
pii: 104057
doi: 10.18632/aging.104057
pmc: PMC7695405
doi:
Substances chimiques
Amyloid beta-Peptides
0
MAPT protein, human
0
Peptide Fragments
0
amyloid beta-protein (1-42)
0
tau Proteins
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
21004-21022Subventions
Organisme : NIA NIH HHS
ID : R01 AG056531
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG062572
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG008051
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS104127
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG056031
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG066512
Pays : United States
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