Fight Aging!

The brain requires a great deal of energy for normal operation. Indeed, parts of the brain, such as the hippocampus, responsible for memory function, clearly operate at the limits of their capacity even in youth. Aging leads to a reduced blood flow to the brain via a number of mechanisms, including heart failure, atherosclerotic narrowing of blood vessels, and loss of capillary density. This has a negative impact on function. Additionally, however, mitochondrial function declines with age. The hundreds of mitochondria present in every cell work to package chemical energy store molecules to power the cell. When this activity falters, it has a similarly negative result on energy-hungry tissues.

A progressive loss of energy provided to cells in the brain, however it comes about, is thought to be one of the contributing causes of neurodegenerative disease. In today's open access paper, researchers discuss the role of mitochondrial dysfunction in one of the common neurodegenerative conditions, Alzheimer's disease. This is an inflammatory condition, in which much of the focus is placed on the formation of toxic protein aggregates, so it is interesting to see how mitochondrial function fits in to this picture. Alzheimer's, like many neurodegenerative conditions, is likely the converging end result of numerous chains of interacting causes and consequences. The Alzheimer's brain is highly dysfunctional, so short of repairing specific forms of dysfunction in isolation and observing the outcome, it is a challenge to identify true contributing causes versus the side-effects of true contributing causes.

Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope

Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca++ homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamics are thus essential processes in the quality control of mitochondria. According to several recent articles, a continual fusion and fission balance of mitochondria is vital in their normal function maintenance. As a result, the shape and function of mitochondria are inextricably linked. This study examines evidence suggesting that mitochondrial dysfunction plays a significant early impact on AD pathology.

Although mitochondrial dysfunction is a typical indication of Alzheimer's disease, it is unclear whether the cellular systems that maintain mitochondrial integrity malfunction, aggravating mitochondrial pathology. Different levels of vigilance and preventive methods are used to reduce mitochondrial damage and efficiently destroy faulty mitochondria to maintain the mitochondrial equilibrium. The form and function of mitochondria are regulated by mitochondrial fusion and fission. In contrast, mitochondrial transit holds mitochondrial dispersion and transports old and damaged mitochondria from distant axons and synapses to the central cell for lysosomal destruction. As the fundamental mechanisms of mitochondrial quality control, several critical properties of mitochondria work in tandem with mitophagy. According to the findings, mitochondrial viability and function are managed by mitochondrial fusion, fission, transport, and mitophagy, forming a complex, dynamic, and reciprocal interaction network.

According to growing evidence, AD brains have disrupted mitochondrial dynamics and aberrant mitophagy, which may interfere with mitochondrial quality control directly or indirectly. Further research into these processes might help us better understand mitochondrial malfunction in Alzheimer's disease. Given the ability to improve some phenotypes by manipulating genes that regulate mitophagy, there is reason to believe that attempting to subvert mitochondrial dynamics, motility unilaterally, and mitophagy will enhance mitochondrial surveillance mechanisms and decrease the neuropathology of Alzheimer's disease, feasibly leading to new treatment strategies.