Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences

التفاصيل البيبلوغرافية
العنوان: Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences
المؤلفون: Jessica M. Sultana, Vinod Sundaramoorthy, Julie D. Atkin
المصدر: Frontiers in Neuroscience
Frontiers in Neuroscience, Vol 9 (2015)
سنة النشر: 2015
مصطلحات موضوعية: amyotrophic lateral sclerosis, Mini Review, lcsh:RC321-571, symbols.namesake, Medicine, Amyotrophic lateral sclerosis, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Secretory pathway, Psychiatry, business.industry, General Neuroscience, Endoplasmic reticulum, Autophagy, Golgi apparatus, medicine.disease, autophagy dysfunction, Vesicular transport protein, symbols, Unfolded protein response, Axoplasmic transport, secretory trafficking inhibition, business, ER stress, Neuroscience, Golgi fragmentation, axonal degeneration
الوصف: Amyotrophic Lateral Sclerosis (ALS) is an invariably fatal neurodegenerative disorder, which specifically targets motor neurons in the brain, brain stem and spinal cord. Whilst the etiology of ALS remains unknown, fragmentation of the Golgi apparatus is detected in ALS patient motor neurons and in animal/cellular disease models. The Golgi is a highly dynamic organelle that acts as a dispatching station for the vesicular transport of secretory/transmembrane proteins. It also mediates autophagy and maintains endoplasmic reticulum (ER) and axonal homeostasis. Both the trigger for Golgi fragmentation and the functional consequences of a fragmented Golgi apparatus in ALS remain unclear. However, recent evidence has highlighted defects in vesicular trafficking as a pathogenic mechanism in ALS. This review summarizes the evidence describing Golgi fragmentation in ALS, with possible links to other disease processes including cellular trafficking, ER stress, defective autophagy, and axonal degeneration.
تدمد: 1662-4548
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e1f088345975795e67456649010ae7b9Test
https://pubmed.ncbi.nlm.nih.gov/26578862Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....e1f088345975795e67456649010ae7b9
قاعدة البيانات: OpenAIRE