» Articles » PMID: 30292840

Widespread Distribution of Tauopathy in Preclinical Alzheimer's Disease

Overview
Journal Neurobiol Aging
Publisher Elsevier
Date 2018 Oct 8
PMID 30292840
Citations 30
Authors
Affiliations
Soon will be listed here.
Abstract

The objective of this study was to examine the distribution and severity of tau-PET binding in cognitively normal adults with preclinical Alzheimer's disease as determined by positive beta-amyloid PET. F-AV-1451 tau-PET data from 109 cognitively normal older adults were processed with 34 cortical and 9 subcortical FreeSurfer regions and averaged across both hemispheres. Individuals were classified as being beta-amyloid positive (N = 25, A+) or negative (N = 84, A-) based on a F-AV-45 beta-amyloid-PET standardized uptake value ratio of 1.22. We compared the tau-PET binding in the 2 groups using covariate-adjusted linear regressions. The A+ cohort had higher tau-PET binding within 8 regions: precuneus, amygdala, banks of the superior temporal sulcus, entorhinal cortex, fusiform gyrus, inferior parietal cortex, inferior temporal cortex, and middle temporal cortex. These findings, consistent with preclinical involvement of the medial temporal lobe and parietal lobe and association regions by tauopathy, emphasize that therapies targeting tauopathy in Alzheimer's disease could be considered before the onset of symptoms to prevent or ameliorate cognitive decline.

Citing Articles

Impact of amygdala functional connectivity on cognitive impairment in Alzheimer's disease.

Kicik A, Kurt E, Hari E, Ulasoglu-Yildiz C, Gurvit H, Demiralp T Neurol Sci. 2025; .

PMID: 40055296 DOI: 10.1007/s10072-025-08091-0.


Plasma Phosphorylated Tau 217 as a Discriminative Biomarker for Cerebral Amyloid Angiopathy.

Hsieh P, Tsai H, Liu C, Lee B, Tsai Y, Yen R Eur J Neurol. 2025; 32(2):e70066.

PMID: 39907306 PMC: 11795418. DOI: 10.1111/ene.70066.


Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by Aβ oligomers.

Zou J, McNair E, DeCastro S, Lyons S, Mordant A, Herring L J Neuroinflammation. 2024; 21(1):215.

PMID: 39218898 PMC: 11367981. DOI: 10.1186/s12974-024-03208-2.


A review of the flortaucipir literature for positron emission tomography imaging of tau neurofibrillary tangles.

Burnham S, Iaccarino L, Pontecorvo M, Fleisher A, Lu M, Collins E Brain Commun. 2024; 6(1):fcad305.

PMID: 38187878 PMC: 10768888. DOI: 10.1093/braincomms/fcad305.


Amidst an amygdala renaissance in Alzheimer's disease.

Stouffer K, Grande X, Duzel E, Johansson M, Creese B, Witter M Brain. 2023; 147(3):816-829.

PMID: 38109776 PMC: 10907090. DOI: 10.1093/brain/awad411.


References
1.
Braak H, Braak E . Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991; 82(4):239-59. DOI: 10.1007/BF00308809. View

2.
Lemoine L, Leuzy A, Chiotis K, Rodriguez-Vieitez E, Nordberg A . Tau positron emission tomography imaging in tauopathies: The added hurdle of off-target binding. Alzheimers Dement (Amst). 2018; 10:232-236. PMC: 5956931. DOI: 10.1016/j.dadm.2018.01.007. View

3.
Schwarz A, Yu P, Miller B, Shcherbinin S, Dickson J, Navitsky M . Regional profiles of the candidate tau PET ligand 18F-AV-1451 recapitulate key features of Braak histopathological stages. Brain. 2016; 139(Pt 5):1539-50. DOI: 10.1093/brain/aww023. View

4.
Lowe V, Curran G, Fang P, Liesinger A, Josephs K, Parisi J . An autoradiographic evaluation of AV-1451 Tau PET in dementia. Acta Neuropathol Commun. 2016; 4(1):58. PMC: 4906968. DOI: 10.1186/s40478-016-0315-6. View

5.
Marquie M, Normandin M, Vanderburg C, Costantino I, Bien E, Rycyna L . Validating novel tau positron emission tomography tracer [F-18]-AV-1451 (T807) on postmortem brain tissue. Ann Neurol. 2015; 78(5):787-800. PMC: 4900162. DOI: 10.1002/ana.24517. View