Perilous Sites: High basic Fibroblast Growth Factor level supplement Parkinson’s disease pathology and its Spread

ABSTRACT: Lewy body (LB) pathology and loss of dopaminergic neurons are imprints of Parkinson’s disease (PD). LBs are mainly comprised of alpha-Synuclein (Dijkstra et al., 2014). Strolling detection of LBs in brain regions contribute to progressive construct of PD pathology to which molecular mechanisms are not clear (H. Braak & Del Tredici, 2017). Two key facets of LB formation are protein aggregation via misfolding and transmission of misfoldled proteins to various brain regions, eventually causing neuronal death (Goedert, Spillantini, Del Tredici, & Braak, 2013; Pacelli et al., 2015). Misfolding requires alterations in intracellular physiology (Carbone, Costa, Provensi, Mannaioni, & Masi, 2017; Funes et al., 2014; Guzman et al., 2018; Pacelli et al., 2015) and detection of misfolded proteins in exosomes confirms exosomatic transmission (Ngolab et al., 2017). High levels of neurotropic-factors (Brockmann et al., 2017) and changes in bioenergetics are found in PD patients, these can bring physiological alterations (Smith et al., 2018). En masse, these evidences and hipocampal association with synucleopathies (Flores-Cuadrado, Ubeda-Bañon, Saiz-Sanchez, de la Rosa-Prieto, & Martinez-Marcos, 2016) allowed us to probe other volunerable PD proteins in cell-lysate and exosomal proteomes of bFGF treated hippocampal neurons. Using WPCNA we developed co-expression modules and spotted many PD related proteins; which can act as precursors during diseased or onset stage.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Primary Cell, Neuron

SUBMITTER: Stephan Mueller  

LAB HEAD: Stefan F. Lichtenthaler

PROVIDER: PXD015969 | Pride | 2020-07-21

REPOSITORIES: Pride