Anavex Life Sciences Corp (AVXL)

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HSP and Mitochondrial Dysfunction

This paper, Hereditary Spastic Paraplegia-Linked REEP1 Modulates ER Mitochondria Contacts, Ann Neurol. 2015 November ; 78(5): 679–696. doi:10.1002/ana.24488, tells of a protein, REEP1, that disrupts the endoplasmic reticulum-mitochondrial connection membranes, the MAMs in HSP.

This information fully supports the ability of Anavex 2-73 to restore those inter-organelle membrane connections, as it does in Alzheimer’s and other CNS diseases.

The paper tells of the causative involvement of MAMs disconnects in CNS diseases:

The physical interactions between the ER and mitochondria play important roles in many aspects of cellular functions. The contact sites, known as mitochondria-associated ER membranes (MAMs), serve as channels for transporting molecules (e.g. membrane lipids, proteins, and Ca2+) between the two organelles and as hubs for mitochondrial fusion/fission and autophagosome formation.17–20 Alterations in ER-mitochondrial contact often leads to mitochondrial dysfunction and compromised ER function.1,2,4,21 Recent evidence suggests that the deregulation of ER-mitochondrial contacts and impaired Ca2+ transfer at such sites is a common pathogenic mechanism in various neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis.

The ability of Anavex 2-73 to restore normal ambulation in those transgenic rats with HSP fits with the information in this paper. Not conjecture by any means. Anavex works, by a well-studied and documented mechanism of action (documented elsewhere).