Dr Shekhar Kedia

Research Associate

My research interests lie in understanding the nanoscale triggers of neurodegenerative disorders using biophysical approaches and how these alterations at the synapses contribute towards the onset of such diseases. It was piqued during my PhD research and continues to grow within postdoctoral research. I am attempting to address the challenges associated with rapid extraction and nanoscale imaging of synapses from brain tissues.

Publications

Hyaluronidase unlocks sequestered CEACAM5 and improves CAR T-cell therapy in colorectal cancer

D Banik, C Ward, Z Zhang, S Chakraborty, D Heraghty, P Suresh, B Li, S Kedia, SJ Davis, JP Roy, MA Chapman, B Mahata, D Klenerman

(2024)

(doi: 10.1101/2024.08.29.610222)

SynPull: a novel method for studying neurodegeneration-related aggregates in synaptosomes using super-resolution microscopy

S Kedia, E Fertan, Y Wu, YP Zhang, G Meisl, JYL Lam, F Wiseman, WA McEwan, A Quaegebeur, MG Spillantini, JSH Danial, D Klenerman

(2024)

(doi: 10.1101/2024.08.24.609517)

The delayed kinetics of Myddosome formation explains why amyloid-beta aggregates trigger Toll-like receptor 4 less efficiently than lipopolysaccharide

B Li, P Suresh, J Brelstaff, S Kedia, CE Bryant, D Klenerman

eLife

(2024)

RP92350

(doi: 10.7554/elife.92350.3)

The delayed kinetics of Myddosome formation explains why amyloid-beta aggregates trigger Toll-like receptor 4 less efficiently than lipopolysaccharide.

B Li, P Suresh, J Brelstaff, S Kedia, CE Bryant, D Klenerman

(2024)

(doi: 10.7554/eLife.92350)

The delayed kinetics of Myddosome formation explains why Aβ aggregates trigger TLR4 less efficiently than LPS

B Li, P Suresh, J Brelstaff, S Kedia, C Bryant, D Klenerman

(2023)

(doi: 10.1101/2023.09.28.559977)

Real-time heterogeneity of supramolecular assembly of amyloid precursor protein is modulated by an endocytic risk factor PICALM.

V Belapurkar, HS Mahadeva Swamy, N Singh, S Kedia, SRG Setty, M Jose, D Nair

Cell Mol Life Sci

(2023)

295

(doi: 10.1007/s00018-023-04939-w)

Golgi fragmentation – One of the earliest organelle phenotypes in Alzheimer’s disease neurons

H Haukedal, GI Corsi, VP Gadekar, NT Doncheva, S Kedia, N de Haan, A Chandrasekaran, P Jensen, P Schiønning, S Vallin, FR Marlet, A Poon, C Pires, FK Agha, HH Wandall, S Cirera, AH Simonsen, TT Nielsen, JE Nielsen, P Hyttel, R Muddashetty, BI Aldana, J Gorodkin, D Nair, M Meyer, MR Larsen, K Freude

Front Neurosci

(2023)

1120086

(doi: 10.3389/fnins.2023.1120086)

Golgi fragmentation - One of the earliest organelle phenotypes in Alzheimer’s disease neurons

(2022)

(doi: 10.1101/2022.12.09.519571)