Mitochondrial Fragmentation as a Key Driver of Neurodegenerative Disease.

Mitochondrial form and function are intricately linked through dynamic processes of fusion and fission, and disruptions in these processes are key drivers of neurodegenerative diseases, like Alzheimer's. The inability of mitochondria to transition between their dynamic forms is a critical factor in the development of pathological states. In this paper, we focus on the importance of different types of mitochondrial phenotypes in nervous tissue, discussing how mitochondria in Alzheimer's disease are "stuck" in certain patterns and how this pattern maintains itself.

Unique Properties of Synaptosomes and Prospects for Their Use for the Treatment of Alzheimer's Disease.

Alzheimer's disease (AD) is a severe neurodegenerative condition affecting millions worldwide. Prevalence of AD correlates with increased life expectancy and aging population in the developed countries. Considering that AD is a multifactorial disease involving various pathological processes such as synaptic dysfunction, neuroinflammation, oxidative stress, and improper protein folding, a comprehensive approach targeting multiple pathways may prove effective in slowing the disease progression.

Intranasal administration of mitochondria improves spatial memory in olfactory bulbectomized mice.

Here, we found that functionally active mitochondria isolated from the brain of NMRI donor mice and administrated intranasally to recipient mice penetrated the brain structures in a dose-dependent manner. The injected mitochondria labeled with the MitoTracker Red localized in different brain regions, including the neocortex and hippocampus, which are responsible for memory and affected by degeneration in patients with Alzheimer's disease. In behavioral experiments, intranasal microinjections of brain mitochondria of native NMRI mice improved spatial memory in the olfactory bulbectomized (OBX) mice with Alzheimer's type degeneration.