Learn how endoplasmic reticulum and mitochondrial dysfunctions contribute to ALS pathophysiology.
Recent progress in the understanding of neurodegenerative diseases revealed that multiple molecular mechanisms contribute to pathological changes in neurons. A large fraction of these alterations can be linked to biochemical dysfunction in the endoplasmic reticulum (ER) and mitochondria — physically and functionally interconnected via mitochondrial-associated membranes (MAM), which participate in Ca2+ signaling, lipid transport, energy metabolism and cell survival. Apart from their vital physical association coordinating pathways involved in cell life and death, any loss of communication in them complicates and worsens the prevailing conditions in neurodegenerative diseases like ALS and Alzheimer’s disease.
While delays in ALS diagnosis are common, early accurate diagnosis by an ALS specialist improves patient care and makes it possible for people to avoid unnecessary procedures and specialist referrals. Early ALS symptoms include muscle weakness, atrophy, spasticity, difficulty speaking, chewing or swallowing, but may vary by patient.
An overview of findings from the clinical trial of AMX0035 for the treatment of Amyotrophic Lateral Sclerosis (ALS).