In vivo coupling of dendritic complexity with presynaptic density in primary tauopathies.

Autor: Mak E; Department of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, UK., Holland N; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK; Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. Electronic address: Nda26@cam.ac.uk., Jones PS; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., Savulich G; Department of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, UK., Low A; Department of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, UK., Malpetti M; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., Kaalund SS; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., Passamonti L; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., Rittman T; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., Romero-Garcia R; Department of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, UK., Manavaki R; Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, UK., Williams GB; Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, UK., Hong YT; Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, UK., Fryer TD; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK; Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, UK., Aigbirhio FI; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK., O'Brien JT; Department of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, UK; Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK., Rowe JB; Department of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK; Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK; Medical Research Council Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Jazyk: angličtina
Zdroj: Neurobiology of aging [Neurobiol Aging] 2021 May; Vol. 101, pp. 187-198. Date of Electronic Publication: 2021 Jan 30.
DOI: 10.1016/j.neurobiolaging.2021.01.016
Abstrakt: Understanding the cellular underpinnings of neurodegeneration remains a challenge; loss of synapses and dendritic arborization are characteristic and can be quantified in vivo, with [ 11 C]UCB-J PET and MRI-based Orientation Dispersion Imaging (ODI), respectively. We aimed to assess how both measures are correlated, in 4R-tauopathies of progressive supranuclear palsy - Richardson's Syndrome (PSP-RS; n = 22) and amyloid-negative (determined by [ 11 C]PiB PET) Corticobasal Syndrome (Cortiobasal degeneration, CBD; n =14), as neurodegenerative disease models, in this proof-of-concept study. Compared to controls (n = 27), PSP-RS and CBD patients had widespread reductions in cortical ODI, and [ 11 C]UCB-J non-displaceable binding potential (BP ND ) in excess of atrophy. In PSP-RS and CBD separately, regional cortical ODI was significantly associated with [ 11 C]UCB-J BP ND in disease-associated regions (p < 0.05, FDR corrected). Our findings indicate that reductions in synaptic density and dendritic complexity in PSP-RS and CBD are more severe and extensive than atrophy. Furthermore, both measures are tightly coupled in vivo, furthering our understanding of the pathophysiology of neurodegeneration, and applicable to studies of early neurodegeneration with a safe and widely available MRI platform.
(Copyright © 2021. Published by Elsevier Inc.)
Databáze: MEDLINE
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