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Updated: Jan 2, 2026
In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
Plasma tau correlates with basal forebrain atrophy rates in people at risk for Alzheimer disease
Enrica Cavedo1, Simone Lista2, Marion Houot2
1From Alzheimer Precision Medicine (APM) (E.C., S.L., A.V., B.D., H.H.), AP-HP, Pitié-Salpêtrière Hospital, Sorbonne University; Brain & Spine Institute (ICM) (E.C., S.L., M.H., A.V., M.C.P., B.D.), INSERM U 1127, CNRS UMR 7225; Institute of Memory and Alzheimer's Disease (IM2A) (E.C., S.L., M.H., A.V., B.D.), Department of Neurology, Pitié-Salpêtrière Hospital, AP-HP; Qynapse (E.C.); Centre of Excellence of Neurodegenerative Disease (CoEN) (M.H.), ICM, CIC Neurosciences, APHP Department of Neurology, Hôpital Pitié-Salpêtrière, Paris, France; German Center for Neurodegenerative Diseases (DZNE)-Rostock/Greifswald (M.J.G., S.T.); Department of Psychosomatic Medicine (M.J.G., S.T.), University of Rostock, Germany; Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry (H.Z.), the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (H.Z., K.B.), London, UK; Laboratoire d'Imagerie Biomédicale (M.-O.H.), Sorbonne Université, CNRS, INSERM; Centre pour l'Acquisition et le Traitement des Images (cati-neuroimaging.com) (M.-O.H.); and Département de Médecine Nucléaire (M.-O.H.), AP-HP, Hôpital Pitié-Salpêtrière, Paris, France. enrica.cavedo@gmail.com.
Objective:
To investigate whether baseline concentrations of plasma total tau (t-tau) and neurofilament light (NfL) chain proteins are associated with annual percent change (APC) of the basal forebrain cholinergic system (BFCS) in cognitively intact older adults at risk for Alzheimer disease (AD).
Methods:
This was a large-scale study of 276 cognitively intact older adults from the monocentric INSIGHT-preAD (Investigation of Alzheimer's Predictors in Subjective Memory Complainers) cohort. Participants underwent baseline assessment of plasma t-tau and NfL concentrations as well as baseline and 24-month follow-up MRI scans. Linear models with and without influential observations (calculated using the Cook distance) were carried out to investigate the effect of plasma NfL and t-tau concentrations, and their interaction effect with β-amyloid status and APOE genotype, on the APC of the whole BFCS and its anterior (Ch1/2) and posterior (Ch4) subdivisions separately.
Results:
Higher plasma t-tau concentrations at baseline were associated with higher BFCS rate of atrophy (model without influencers: n = 251, F value = 4.6815; p value = 0.031). Subregional analyses showed similar results for both the APC of the Ch1/2 (model without influencers: n = 256, F value = 3.9535, p corrected = 0.047) and Ch4 BFCS sectors (model without influencers: n = 253, F value = 4.9090, p corrected = 0.047). Baseline NfL, β-amyloid load, and APOE ε4 carrier status did not affect APC of the BFCS.
Conclusion:
Increased concentrations of baseline plasma t-tau may predict in vivo structural BFCS atrophy progression in older adults at risk for AD, independently of β-amyloid status and APOE genotype.
