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Electromagnetic radiation (EMR) can induce or modulate several neurobehavioral disorders. Duration and frequency of exposure of EMR is critical to develop cognitive disorders. Even though EMR-2450 is widely used, its effects on cognition in relation to mitochondrial function and apoptosis would provide better understanding of its pathophysiological effects. Therefore, a comparative study of different frequencies of EMR exposure would give valuable information on effects of discrete frequencies of EMR on cognition. Male rats were exposed to EMR (900, 1800 and 2450 MHz) every day for 1 h for 28 consecutive days. The cognitive behavior in terms of novel arm entries in Y-maze paradigm was evaluated every week after 1 h to last EMR exposure. Animals exposed to EMR-2450 MHz exhibited significant cognitive deficits. EMR-2450 MHz caused loss of mitochondrial function and integrity, an increase in amyloid beta expression. There was release of cytochrome-c and activation of apoptotic factors such as caspase-9 and -3 in the hippocampus. Further, there was decrease in levels of acetylcholine, and increase in activity of acetyl cholinesterase, indicating impairment of cholinergic system. Therefore, exposure of EMR-2450 in rats caused cognitive deficit with related pathophysiological changes in mitochondrial and cholinergic function, and amyloidogenesis. [ABSTRACT FROM AUTHOR]

Alzheimer's Disease (AD) remains a formidable challenge due to its complex pathology, notably involving mitochondrial dysfunction and dysregulated microRNA (miRNA) signaling. This study delves into the underexplored realm of miRNAs' impact on mitochondrial dynamics and their interplay with amyloid-beta (Aβ) aggregation and tau pathology in AD. Addressing identified gaps, our research utilizes advanced molecular techniques and AD models, alongside patient miRNA profiles, to uncover miRNAs pivotal in mitochondrial regulation. We illuminate novel miRNAs influencing mitochondrial dynamics, Aβ, and tau, offering insights into their mechanistic roles in AD progression. Our findings not only enhance understanding of AD's molecular underpinnings but also spotlight miRNAs as promising therapeutic targets. By elucidating miRNAs' roles in mitochondrial dysfunction and their interactions with hallmark AD pathologies, our work proposes innovative strategies for AD therapy, aiming to mitigate disease progression through targeted miRNA modulation. This contribution marks a significant step toward novel AD treatments, emphasizing the potential of miRNAs in addressing this complex disease. • miRNAs regulate key AD pathologies. • Aβ, tau impact on neuronal health. • Novel miRNA-based therapies explored. • Challenges in miRNA therapy delivery. • Future: personalized AD treatments. [ABSTRACT FROM AUTHOR]