Anavex Life Sciences Corp (AVXL)

[polarbear77]

Excellent points, and this seemed also on topic:

http://cdn.intechopen.com/pdfs-wm/48230.pdf
Published 2015

Excerpts:
“Mitochondria are sub-cellular organelles that play pivotal roles essential for energy (ATP) production, metabolism, and homeostasis.”

“Investigation associating an elevated oxidant state with mitochondrial damage, aging dictates, and degenerative disease the need for a better under- standing of how and when pharmacological manipulation of mitochondrial function prepares most therapeutic benefit [4].

Mitochondria carry out vital biochemical functions essential for cells such as homeostasis calcium, cell death and survival, in addition to ATP production.”

“Furthermore, mitochondria are active players in cellular calcium homeostasis. Mitochondrial Ca2+ accumulation regulates functions as diverse as aerobic metabolism and induction of cell death. Finally, mutations in mitochondrial DNA (mtDNA) are responsible for many mitochondrial metabolic disorders, and are thought to contribute to aging by promoting apoptosis.”

“...degenerative and aging diseases are associated with an elevated oxidant state that may associate mitochondrial damage. In these cases, antioxidants targeting mitochondria are hoped to exert a justifying effect. Several studies are found in this category, all sharing the common features of disturbances of mitochondrial ROS, ATP or Ca2+ metabolism. They contain cardiovascular diseases (for example atherosclerosis, ischemia/reperfusion injury, heart failure, stroke); aging and neurodegenerative diseases (for example Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS) and Friedreich’s ataxia (FRDA)); chronic autoimmune inflammatory diseases (for example rheumatoid arthritis (RA)) ; metabolic diseases(for example diabetes and obesity) ; as well as ionizing radiation injury (Table 1) [6].”

“Small molecule drugs or biologics can act on mitochondria through various pathways. Many of these mechanisms will be argued in more detail in the below sections, and a detailed discussion would immensely encroach the purpose of this chapter, but attractive current approaches include OXPHOS uncoupling, mitochondrial Ca2+ modulation, ETC inhibition and control of oxidative stress through increase or decrease of mitochondrial ROS accumulation.”