<i>Post mortem</i> validation and mechanistic study of UCB‐J in progressive supranuclear palsy patients’ brains

UCB-J targeted synaptic vesicle protein 2A with high specificity in progressive supranuclear palsy (PSP) brains and demonstrated a conserved single nM binding site across different brain regions. UCB-J depicted prominent synaptic loss at the synaptosome levels and revealed deficits of glutamate/GABAergic synaptic terminals in the early affected globus pallidus of PSP brains as compared to the control. Cortical and subcortical 4R tau load distinctly influenced synaptic markers profile across PSP patients and highlighted that presynaptic "ubiquitous" markers individually might not be able to represent the complete state of synaptic deficits/loss in PSP brains.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2024-12-13
DOI
https://doi.org/10.1002/alz.14409
Citations
2
Primary Topic
Parkinson's Disease Mechanisms and Treatments
Type
article
Field-Weighted Citation Impact
0.74

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article

Post mortem validation and mechanistic study of UCB‐J in progressive supranuclear palsy patients’ brains

Miriam Scarpa, Amit Kumar, Avishek Roy, Sira Ausellé‐Bosch et al.
2 citations
Alzheimer s & Dementia
Parkinson's Disease Mechanisms and Treatments
0.74
article

Post mortem validation and mechanistic study of UCB‐J in progressive supranuclear palsy patients’ brains

Miriam Scarpa, Amit Kumar, Avishek Roy, Sira Ausellé‐Bosch, Agneta Nordberg, Filipa M. Rocha, Elisavet Vallera, Buse Esra Mercan
article en
2 citations

Abstract

UCB-J targeted synaptic vesicle protein 2A with high specificity in progressive supranuclear palsy (PSP) brains and demonstrated a conserved single nM binding site across different brain regions. UCB-J depicted prominent synaptic loss at the synaptosome levels and revealed deficits of glutamate/GABAergic synaptic terminals in the early affected globus pallidus of PSP brains as compared to the control. Cortical and subcortical 4R tau load distinctly influenced synaptic markers profile across PSP patients and highlighted that presynaptic "ubiquitous" markers individually might not be able to represent the complete state of synaptic deficits/loss in PSP brains.

Alzheimer s & DementiaVol. 21(2)
Karolinska University Hospital (SE), University of Crete (GR), Universitat de Girona (ES), Karolinska Institutet (SE), Hacettepe University (TR)
Gun och Bertil Stohnes Stiftelse, Loo och Hans Ostermans Stiftelse för Medicinsk Forskning, Tore Nilsons Stiftelse för Medicinsk Forskning, Stiftelsen för Strategisk Forskning, Fondation pour la Recherche Médicale, Hjärnfonden, Karolinska Institutet, Stockholms Läns Landsting, Vetenskapsrådet, Magnus Bergvalls Stiftelse, Alzheimerfonden, Demensfonden, Center for Innovative Medicine
Openalex Percentile: Top 25%
Parkinson's Disease Mechanisms and Treatments
0.74
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<i>Post mortem</i> validation and mechanistic study of UCB‐J in progressive supranuclear palsy patients’ brains — Miriam Scarpa, Amit Kumar, et al. · Alzheimer s & Dementia (2024) | TGRS Research Map | TGRS