Alzheimer's disease (AD) is the most common form of dementia, affecting millions of individuals each year and this number is expected to significantly increase. The complicated microorganisms residing in human gut are closely associated with our health. Emerging evidence has suggested possible involvement of human gut microbiome in AD. Symbiotic gut microbiomes are known to maintain brain health by modulating host's barriers integrity, metabolic system, immune system, nervous system and endocrine system. However, in the event of gut dysbiosis and barriers disruption, gut pathobionts disrupt homeostasis of the metabolic system, immune system, nervous system, and endocrine system, resulting in deterioration of neurological functions and subsequently promoting development of AD. Multiple therapeutic approaches, such as fecal microbiome transplant, antibiotics, prebiotics, probiotics, symbiotic, and diet are discussed as potential treatment options for AD by manipulating the gut microbiome to reverse pathological alteration in the systems above.
Neurodegenerative diseases represent a significant challenge to modern medicine, with their complex etiology and progressive nature posing hurdles to effective treatment strategies. Among the various contributing factors, mitochondrial dysfunction has emerged as a pivotal player in the pathogenesis of several neurodegenerative disorders. This review paper provides a comprehensive overview of how mitochondrial impairment contributes to the development of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, driven by bioenergetic defects, biogenesis impairment, alterations in mitochondrial dynamics (such as fusion or fission), disruptions in calcium buffering, lipid metabolism dysregulation and mitophagy dysfunction. It also covers current therapeutic interventions targeting mitochondrial dysfunction in these diseases.
Major depressive disorder (MDD) patients commonly encounter multiple types of functional disabilities, such as social, physical, and role functioning. MDD is related to an accreted risk of brain atrophy, aging-associated brain diseases, and mortality. Based on recently available studies, there are correlations between notable biological brain aging and MDD in adulthood. Despite several clinical and epidemiological studies that associate MDD with aging phenotypes, the underlying mechanisms in the brain remain unknown. The key areas in the study of biological brain aging in MDD are structural brain aging, impairment in functional connectivity, and the impact on cognitive function and age-related disorders. Various measurements have been used to determine the severity of brain aging, such as the brain age gap estimate (BrainAGE) or brain-predicted age difference (BrainPAD). This review summarized the current results of brain imaging data on the similarities between the manifestation of brain structural changes and the age-associated processes in MDD. This review also provided recent evidence of BrainPAD or BrainAGE scores in MDD, brain structural abnormalities, and functional connectivity, which are commonly observed between MDD and age-associated processes. It serves as a basis of current reference for future research on the potential areas of investigation for diagnostic, preventive, and potentially therapeutic purposes for brain aging in MDD.