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Alzheimer's disease (AD) is a devastating neurodegenerative disorder that affects millions of people worldwide. It is characterized by the accumulation of beta-amyloid and phosphorylated tau, synaptic damage, and mitochondrial abnormalities in the brain, leading to the progressive loss of cognitive function and memory. In AD, emerging research suggests that lifestyle factors such as a healthy diet and regular exercise may play a significant role in delaying the onset and progression of the disease. Mitochondria are often referred to as the powerhouse of the cell, as they are responsible for producing the energy to cells, including neurons to maintain cognitive function. Our article elaborates on how mitochondrial quality and function decline with age and AD, leading to an increase in oxidative stress and a decrease in ATP production. Decline in mitochondrial quality can impair cellular functions contributing to the development and progression of disease with the loss of neuronal functions in AD. This article also covered mitophagy, the process by which damaged or dysfunctional mitochondria are selectively removed from the cell to maintain cellular homeostasis. Impaired mitophagy has been implicated in the progression and pathogenesis of AD. We also discussed the impact of impaired mitophagy implicated in AD, as the accumulation of damaged mitochondria can lead to increased oxidative stress. We expounded how dietary interventions and exercise can help to improve mitochondrial quality, and mitochondrial function and enhance mitophagy in AD. A diet rich in antioxidants, polyphenols, and mitochondria-targeted small molecules has been shown to enhance mitochondrial function and protect against oxidative stress, particularly in neurons with aged and mild cognitively impaired subjects and AD patients. Promoting a healthy lifestyle, mainly balanced diet and regular exercise that support mitochondrial health, in an individual can potentially delay the onset and progression of AD. In conclusion, a healthy diet and regular exercise play a crucial role in maintaining mitochondrial quality and mitochondrial function, in turn, enhancing mitophagy and synaptic activities that delay AD in the elderly populations.
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http://dx.doi.org/10.1016/j.arr.2025.102734 | DOI Listing |
Diabetes Metab Syndr Obes
September 2025
School of Medical, Indigenous and Health, University of Wollongong, Wollongong, New South Wales, Australia.
Introduction: Obesity remains a critical global health challenge, intricately linked to poor dietary quality, gut microbiota dysbiosis, and mitochondrial dysfunction.
Purpose: This study aimed to investigate the comparative effects of brown rice, meal replacements, and thiazolidinediones on mitochondrial abundance and gut microbiota composition in a rat model of diet-induced obesity.
Methods And Materials: A total of twenty male Sprague Dawley rats were randomly assigned to five groups: control, high-fat high-fructose diet, and three intervention groups receiving the same obesogenic diet supplemented with brown rice, meal replacement, or thiazolidinediones for twelve weeks.
Diabetes Metab Syndr Obes
September 2025
Medical School, Kunming University of Science and Technology, Kunming, People's Republic of China.
Diabetes has emerged as a critical global health issue, with its associated complications posing a severe threat to patients' quality of life. Current research demonstrates that imbalance in mitochondrial dynamics and autophagic dysregulation play pivotal roles in the pathogenesis of diabetic complications, particularly in diabetic cardiomyopathy, nephropathy, peripheral neuropathy and retinopathy. Strategic modulation of mitochondrial function and autophagic activity represents a promising therapeutic approach for managing diabetic complications.
View Article and Find Full Text PDFMedComm (2020)
September 2025
The activation of nucleotide oligomerization domain-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome is implicated in the pathogenesis of various inflammatory diseases. The natural product oridonin possesses a novel mechanism for NLRP3 inhibition and a unique binding mode with NLRP3, but its poor anti-inflammatory activity limits further application. After virtual screening of diverse natural product libraries, dehydrocostus lactone (DCL) was considered as a potential NLRP3 inhibitor.
View Article and Find Full Text PDFFront Pharmacol
August 2025
Department of Pharmacy, Zigong Maternal and Child Health Care Hospital, Zigong, China.
This review comprehensively summarizes the current understanding of ubiquitin-specific protease 30 (USP30), covering its structural characteristics, functions in cellular processes, associations with diseases, diagnostic and therapeutic strategies, as well as controversies and future perspectives. USP30, a deubiquitinating enzyme, plays crucial roles in mitochondrial quality control, autophagy regulation, and cellular homeostasis. It is implicated in the progression of several malignancies, including hepatocellular carcinoma, breast carcinoma, and glioblastoma, as well as neurodegenerative disorders such as Parkinson's disease.
View Article and Find Full Text PDFAging is associated with cognitive decline, impaired spatial learning, and diminished brain function, significantly impacting quality of life (QoL). Emerging evidence suggests that lifestyle interventions, like omega-3 fatty acids (FAs) intake and regular exercise, can mitigate these age-related deficits by targeting key molecular pathways implicated in oxidative damage, inflammation, and reduced fibrinolytic activity. By doing so, omega-3 FAs, principally eicosapentaenoic acid and docosahexaenoic acid, influence signaling pathways that enhance synaptic plasticity, prevent apoptosis, and promote neurogenesis.
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