Check of a new non-perturbative mechanism for elementary fermion mass generation

We consider a field theoretical model where a SU(2) fermion doublet, subjected to non-Abelian gauge interactions, is also coupled to a complex scalar field doublet via a Yukawa and an irrelevant Wilson-like term. Despite the presence of these two chiral breaking operators in the Lagrangian, an exact symmetry acting on fermions and scalars prevents perturbative mass corrections. In the phase where fermions are massless (Wigner phase) the Yukawa coupling can be tuned to a critical value at which chiral transformations acting on fermions only become a symmetry of the theory (up to cutoff effects). In the Nambu-Goldstone phase of the critical theory a fermion mass term of dynamical origin is expected to arise in the Ward identities of the purely fermionic chiral transformations. Such a non-perturbative mechanism of dynamical mass generation can provide a "natural" (\`a la 't Hooft) alternative to the Higgs mechanism adopted in the Standard Model. Here we lay down the theoretical framework necessary to demonstrate the existence of this mechanism by means of lattice simulations.Comment: 7 pages, 3 figureres, Proceedings for The 34th International Symposium on Lattice Field Theor

Blood RNA biomarkers in prodromal PARK4 and apid eye movement sleep behavior disorder show role of complexin-1 loss for risk of Parkinson's disease

Parkinson's disease (PD) is a frequent neurodegenerative process in old age. Accumulation and aggregation of the lipid-binding SNARE complex component α-synuclein (SNCA) underlies this vulnerability and defines stages of disease progression. Determinants of SNCA levels and mechanisms of SNCA neurotoxicity have been intensely investigated. In view of the physiological roles of SNCA in blood to modulate vesicle release, we studied blood samples from a new large pedigree with SNCA gene duplication (PARK4 mutation) to identify effects of SNCA gain of function as potential disease biomarkers. Downregulation of complexin 1 (CPLX1) mRNA was correlated with genotype, but the expression of other Parkinson's disease genes was not. In global RNA-seq profiling of blood from presymptomatic PARK4 indviduals, bioinformatics detected significant upregulations for platelet activation, hemostasis, lipoproteins, endocytosis, lysosome, cytokine, Toll-like receptor signaling and extracellular pathways. In PARK4 platelets, stimulus-triggered degranulation was impaired. Strong SPP1, GZMH and PLTP mRNA upregulations were validated in PARK4. When analysing individuals with rapid eye movement sleep behavior disorder, the most specific known prodromal stage of general PD, only blood CPLX1 levels were altered. Validation experiments confirmed an inverse mutual regulation of SNCA and CPLX1 mRNA levels. In the 3′-UTR of the CPLX1 gene we identified a single nucleotide polymorphism that is significantly associated with PD risk. In summary, our data define CPLX1 as a PD risk factor and provide functional insights into the role and regulation of blood SNCA levels. The new blood biomarkers of PARK4 in this Turkish family might become useful for PD prediction