The Kinase Fyn As a Novel Intermediate in l-DOPA-Induced Dyskinesia in Parkinson’s Disease

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

“…PD is thought to display prion-like pathogenesis at least in part by the misfolding characteristics and intercellular spread of SNCA; this was exemplified by the spread of Lewy pathology into healthy donor brain cells that were grafted into the striatum of PD patients. 88,89 With respect to PD pathogenesis, the information we have so far about these proteins is limited and not necessarily associated with prions: neural cell adhesion molecule 1 have been shown to regulate dopaminergic signaling and behavior by regulating dopamine receptor internalization 90 ; FYN Proto-Oncogene has been shown to mediate levodopa-induced dyskinesia 91 and regulate misfolded α-synuclein uptake and inflammasome activation in microglia 92 ; NOTCH signaling is required for the expansion and differentiation of dopaminergic neurons 93 ; prion protein mutations have been found responsible for atypical parkinsonism 94 ; and ELK1 is found in glial cytoplasmic inclusions in multiple system atrophy, and SNCA forms a complex with Elk1, attenuating its phosphorylation and prosurvival signaling in neurons. 95 "TGF-β superfamily signaling pathway" has been shown to control dopaminergic neuron development and survival.…”

“…With respect to PD pathogenesis, the information we have so far about these proteins is limited and not necessarily associated with prions: neural cell adhesion molecule 1 have been shown to regulate dopaminergic signaling and behavior by regulating dopamine receptor internalization; FYN Proto‐Oncogene has been shown to mediate levodopa‐induced dyskinesia and regulate misfolded α‐synuclein uptake and inflammasome activation in microglia; NOTCH signaling is required for the expansion and differentiation of dopaminergic neurons; prion protein mutations have been found responsible for atypical parkinsonism; and ELK1 is found in glial cytoplasmic inclusions in multiple system atrophy, and SNCA forms a complex with Elk1, attenuating its phosphorylation and prosurvival signaling in neurons …”

Fyn Tyrosine Kinase as Harmonizing Factor in Neuronal Functions and Dysfunctions

“…Consistently, Fyn-mediated α-synuclein phosphorylation at Tyr125 was inhibited by the TyrKI inhibitor, PP2 [ 226 ]. In addition, studies performed in Fyn KO mice have prospected the possibility to use Fyn TK inhibitors to prevent or recover the altered dopamine-dependent trafficking of striatal NMDAR observed in PD neurons [ 227 ].…”

Acoustic white noise ameliorates reduced regional brain expression of CaMKII and ΔFosB in the spontaneously hypertensive rat model of ADHD

“…Further, to block endogenous peroxidase activity free floating sections were quenched in PBS containing 3% H 2 O 2 and 10% methanol during gentle agitation. Sections were thereafter first pre-incubated in 5% normal horse or goat serum (Vector laboratories, Burlingame, CA) containing 0.25% Triton-X in PBS, followed by overnight incubation with well-established and specific primary antibodies against either CaMKIIα (mouse, 1: 2000; ab22609; 6G9; Abcam, Cambridge, UK; Jarome et al, 2013; Zhong et al, 2014; Tada et al, 2016; Leroy et al, 2017; Roy et al, 2017) or ΔFosB (Rabbit, 1:5000; SC-48X; Santa Cruz Biotechnology, Dallas, Tx; Djakovic et al, 2012; Sanz-Blasco et al, 2018). On the second day sections were incubated using an appropriate biotinylated secondary antibody (1:250 horse anti mouse BA2001 for CaMKIIα and 1:250 goat anti rabbit BA1000 for ΔFosB; Vector Laboratories,) for one hour followed by one hour incubation in avidin-biotin peroxidase in PBS (ABC Elite Kit, Vector Laboratories).…”