The epidemiology of Alzheimer’s disease (AD) is notable. North America and Western Europe have the most expressive rates of disease (6.4% and 5.4% at age 60), followed by Latin America (4.9%) and, finally China (4%). The most important fact is that head trauma increases the deposition of amyloid βeta (Aβ) and the expression of neuronal tau as well as diabetes. Obesityand trans fats also increase the risk of AD. However, virtually no current pharmacotherapy is approved for agitation / excitation caused by AD, the only purpose is maintaining the memory of those affected by this disease. There is substantial evidence that some dysfunctions in the mitochondria are involved in AD. Mitochondria are essential for neuronal function because the limited glycolytic metabolism of these cells makes them highly dependent on aerobic oxidative phosphorylation (OXPHOS) for their energy needs. Increased concentrations of ROS are known to result in molecular damage to the site where they are produced, triggering what science calls oxidative stress. Another no less important pathophysiological process in neurological disease is mitochondrial membrane cholesterol. New evidence indicates that the burden of mitochondrial cholesterol can influence mitochondrial function regardless of its conversion to pregnenolone or oxysterols, emerging as a key factor in the pathology of several neurological diseases associated with mitochondrial dysfunction, as in the case of AD. In this way, neurons are strictly dependent on the presence of healthy mitochondria, especially in the synapses where these organelles produce ATP and concentration of Ca2 + ions, fundamental processes for the implementation of neurotransmission and generation of membrane potential along the axon. Controlling ROS, as well as reducing the inflammatory cascade in neurons can be a good strategy in controlling the disease. The reduction of cholesterol in the external mitochondrial membrane may be another interesting path for the reentry of glutathione in the control of ROS, which occurs due to the imbalance in the metabolism of the mitochondrial respiratory chain seen in AD. In this review, we discuss the role of mitochondria in AD as well as alternative therapies for controlling this disease with specific herbal and nutraceuticals.
Corrigendum to “Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation” [Redox Biol. 2021 45 102052]
