Most middle-aged and older adult patients with isolated (idiopathic) REM sleep behavior disorder (RBD) eventually develop parkinsonism, dementia with Lewy bodies, or multiple system atrophy. https://doi.org/10.1016/j.sleep.2020.12.014
Specialist Approaches to Prognostic Counseling in Isolated REM Sleep Behavior Disorder Read More »
Background Hypomethylation of intron 1 of the α‐synuclein (SNCA) gene has been extensively reported in the blood of patients with α‐synucleinopathies. Idiopathic rapid eye movement sleep behavior disorder represents a prodromal stage of α‐synucleinopathies. Methylation of α‐synuclein intron 1 in idiopathic rapid eye movement sleep behavior disorder patients is largely unexplored. The objective of the
Functional changes in PNS and ENS appear early in the course of the disease and are responsible for some of the non-motor symptoms observed in PD patients like constipation, that can precede the appearance of motor symptoms by years. We have shown that environmental toxins can trigger the disease by acting on the ENS and
Parkinson’s disease is associated with the formation of protein aggregates called amyloid fibrils. α-synuclein amyloid accumulation is known to be a key factor in the development of neuronal degenerative diseases in the brain, and exploring some toxic compounds with biomedical application like copper oxide (CuO) nanoparticles that can promote protein aggregation and underlying cytotoxicity are
Recent studies highlight the initiation of Parkinson’s disease (PD) in the gastrointestinal tract, decades before the manifestations in the central nervous system (CNS). This gut-brain axis of neurodegenerative diseases defines the critical role played by the unique microbial composition of the “second brain” formed by the enteric nervous system (ENS) https://doi.org/10.1016/j.chemphyslip.2020.105029
Gut-Brain Axis in Parkinson’s disease Etiology: The Role of Lipopolysaccharide Read More »
The ketogenic diet (KD) can promote the anti-inflammatory metabolic state and increase ketone body level in rats. This study was to explore the effects and differences of KD with or without medium-chain fatty acids (MCFAs) on serum inflammatory factors and mTOR pathway in Sprague–Dawley (SD) rats. https://doi.org/10.1186/s40538-020-00194-4
Mitochondrial dysfunction has been associated with neurodegeneration in Parkinson’s disease (PD) for over 30 years. Despite this, the role of mitochondrial dysfunction as an initiator, propagator, or bystander remains undetermined. The discovery of the role of the PD familial genes PTEN-induced putative kinase 1 ( PINK1) and parkin ( PRKN) in mediating mitochondrial degradation (mitophagy) reaffirmed the