Topic: LC3

The primary and progressive degeneration of motor system is the main pathogenic process that characterizes amyotrophic lateral sclerosis (ALS), which is a fatal neurodegenerative disease of motor neurons (MN) in the primary motor cortex and spinal cord. Patients’ death occurs in 3–5 years after the diagnosis due to the progressive palsy and dysfunction of the respiratory system. The etiology is known in most of the patients with the most frequent sporadic ALS (90%), and clinical onset and symptoms are highly heterogeneous. Irrespective of the cause and initial onset the ALS is an almost select

Amyotrophic Lateral Sclerosis (ALS) is an almost selective motoneuron (MN) neurodegenerative disease in which the factors determining preferential involvement of MN are yet to be fully understood. TDP-43 nuclear clearance and aggregates are identified as a major component of the ubiquitinated neuronal cytoplasmic inclusions deposited in spinal motor neurons both in familiar and sALS patients. Since TDP43 protein contains the HSC70 recognition motif, and, therefore, chaperon mediated autophagy (CMA) function may represent a cellular mechanism to regulate TDP43 cytoplasmic turnover in cells. We

Diabetes is a common metabolic disease whose hyperglycemic state can induce various complications, including central nervous system complications. There is evidence which suggests that oxidative stress has a key role in the pathogenesis of diabetes and its complications. Autophagy is one of the main routes to eliminate damaged components in cells in response to oxidative stress. However, excessive autophagy causes a distinct type of cell death involved in the pathogenesis of multiple diseases, such as diabetes. This study aimed to investigate the effect of melatonin on the autophagy in the pre

Mitochondrial dysfunction has been detected in the brains of patients with autism spectrum disorders (ASD) with unclear mechanisms. We herein identify that G protein-coupled receptor 50 (GPR50), which harbors two variations in male ASD patients at Δ502-505 and T532A, is required in mitophagy. GPR50, which does not distribute endogenously in the mitochondrion, is recruited to the damaged mitochondrion, where it marks the mitochondrial portion and recruits the assembling autophagosomes, eventually facilitating itself with the mitochondrial fragments to the autophagosomes. The above process is as

Neurotoxins are numerous groups of drugs that lead detrimental effects on the neuronal system and caused the cognitive and neurological impairments. Intracellular signaling and homeostasis can disturb by those toxins. Lysosomes are crucial organelles to digest waste disposal and supply the essential materials. It is still unknown to connection between lysosomal homeostasis and neurological dysfunction. Here, we investigated how to attenuate the neurodegeneration though managing lysosomal function. After treatment of hydroperoxide as known as one of the neurotoxins, N2A cell proliferation decre