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Therapeutic Effects of Light Flicker Stimulation in a Mouse Model of Depression - A Comparative Study /

By Hyder, Azan . . 80p. , Depression is a common neuropsychiatric condition, characterized by behavioral deficiencies, mood swings, and cognitive impairments. Although fluoxetine is still a commonly prescribed antidepressant, its drawbacks, including systemic side effects and delayed therapeutic results, make it necessary to look at alternative treatments. Using a chronic restraint stress mouse model, this study examines the effectiveness of 40 Hz light flicker therapy as a novel, non-invasive neuromodulatory treatment for depression by directly contrasting it with fluoxetine treatment. Behavioral tests such as the Light-Dark Box, Forced Swim, and Sucrose Preference tests showed that 40 Hz light stimulation dramatically reduced depressive-like behaviors, frequently outperforming the effects of fluoxetine. Histopathological examinations showed that parvalbuminexpressing interneurons, which are necessary for gamma oscillatory activity and inhibitory circuitry, had been protected in the prefrontal cortex (PFC) and hippocampal regions. Increased expression of brain-derived neurotrophic factor (BDNF) and parvalbumin (PV) was further validated by molecular experiments, suggesting improved interneuron integrity and neuroplasticity. These results demonstrate that 40 Hz light flicker therapy facilitates the functional restoration of brain regions damaged in depression, pointing to distinct mechanisms from those of traditional medication. Subsequent research endeavors ought to concentrate on refining stimulation parameters, evaluating long-term safety and effectiveness, and clarifying electrophysiological mechanisms via supplementary imaging and neurophysiological studies. Promising translational potential is indicated by ongoing clinical investigations. To conclude, 40 Hz light flicker therapy might prove to be a useful supplement or substitute therapy, providing a customized, side-effect-free choice for managing depression. 30cm.

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Therapeutic Effects of Sound-Mediated Stimulation in a Mouse Model of Depression - A Comparative Study /

By Reemaz, Tooba . . 90p. , Depression is a prevalent neuropsychiatric disorder characterized by mood disturbances, cognitive impairment, and behavioral deficits. While pharmacological treatments such as Fluoxetine are widely used, they often represent limitations including delayed onset of action and side effects, highlighting the need for alternative, non-invasive therapeutic strategies. One promising approach is neuromodulation through gamma entrainment using auditory stimulation, aimed at restoring disrupted neuronal synchronization. This study evaluates the effects of 40 Hz sound stimulation compared to fluoxetine in a chronic restraint stress-induced mouse model of depression, hypothesizing that sound therapy will yield superior recovery outcomes. Mice were divided into control, depressed, fluoxetine-treated, and sound stimulation-treated groups. Behavioral assessments, including the Tail Suspension Test, Forced Swim Test, Social Interaction Test, Sucrose Preference Test, Open Field Test, and Light-Dark Box Test, revealed that 40 Hz sound therapy significantly alleviated depressive-like behaviors, often outperforming fluoxetine. Histopathological analysis focused on the hippocampus and prefrontal cortex showed that sound stimulation preventing neuronal loss and parvalbumin-expressing interneurons, which are crucial for inhibitory circuit function and gamma oscillatory activity. Molecular evaluation through qPCR for pavlb and brain-derived neurotrophic factor; BDNF supported these findings, displaying increased expression levels indicating enhanced interneuron integrity and neuroplasticity. This neuromodulatory treatment encourages the molecular and functional repair of brain circuitry implicated in depression. The findings demonstrated 40 Hz sound entrainment's ability to change brain oscillations and ameliorate cellular and behavioral deficiencies linked to depression, indicating that it may be a novel supplement or substitute for traditional antidepressant treatments. 30cm.

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Evaluating the Synergistic Role of Insulin and Photobiomodulation in alleviating Diabetic Neuropathy and Cognitive Impairment /

By Kayani, Hooreen . . 88p. , Diabetic neuropathy and cognitive impairment are debilitating complications of diabetes, yet effective multi-targeted therapies remain limited. This study investigated the synergistic effects of Insulin and Photobiomodulation (PBM) in a streptozotocin (STZ) induced diabetic mouse model. Mice were divided into five groups: healthy control, diseased, PBM-treated, Insulintreated, and PBM + Insulin-treated, and received treatments for seven days. Functional outcomes were assessed through behavioural and biochemical analyses, while histopathological and molecular evaluations examined tissue integrity and the expression of neuroprotective markers, including Brain-derived Neurotrophic Factor (BDNF) and Myelin Protein Zero (MPZ), with β-actin as a reference. The combination of PBM and Insulin produced the most pronounced improvements, demonstrating enhanced cognitive performance, reduced neuropathic pain, and preservation of neuronal structure, peripheral nerve integrity, and multi-organ morphology, including the brain, sciatic nerve, heart, liver, kidney, and lungs. PBM or Insulin alone provided partial protection, with moderate amelioration of functional deficits and tissue pathology. Mechanistically, combination therapy upregulated BDNF and MPZ expression, suggesting a molecular basis for enhanced neuroprotection and remyelination. These findings highlight the potential of PBM combined with Insulin as a synergistic intervention to mitigate diabetes-induced neuropathy and cognitive decline. Incorporating such multi-modal strategies may offer a promising avenue for managing diabetes-related multi-organ complications and improving overall outcomes in diabetic patients. 30cm.

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CDCA-Bound Carbon-Based Nanoparticles for the Treatment of Cognitive Impairment and Neuropathy Associated with Diabetes Mellitus /

By Noreen, Samra . . 99p. , Diabetes Mellitus (DM) is a severe metabolic disorder defined by hyperglycemia, which leads to cognitive impairment and neuropathy. It is characterized by chronic pain, sensory loss, impaired motor coordination, and cognitive decline. According to the WHO (2024) and International Diabetes Federation (IDF) statistics, neuropathy affects over 50% of people with type 1 and type 2 diabetes. Current treatments for diabetic neuropathy provide only partial relief and fail to stop neurodegeneration, highlighting the need for novel strategies that both restore metabolic balance and protect neural function. Chenodeoxycholic acid (CDCA), a primary bile acid with antiinflammatory and neuroprotective effects, is limited by toxicity at high doses. CDs, owing to their ultra-small size, biocompatibility, and blood-brain barrier (BBB) permeability, are ideal for treating diabetic neuropathy and cognitive impairment. N-doped CDs were synthesized hydrothermally and conjugated with CDCA via carbodimide coupling. FTIR confirmed preserved functional groups, while UV-Vis showed π–π stacking and hydrogen bonding. Hemocompatibility testing revealed <5% hemolysis, confirming blood safety. Drug loading efficiency was ~ 99.6% (2489.82 bound from 2500 µg). Sustained release analysis showed ~ 17% release at 24 h and ~ 29% over 7 days without a burst effect. In-vivo, diabetic mice were grouped into control, free CDCA, CDCA-NCDs, and insulin glargine. The nanoconjugate was administered at a dose of 10 mg/kg on day 1 st, 7th and 14th compared to daily free CDCA. Behavioral tests (nociception, anxiety, and cognition) showed significant improvements (p < 0.05-0.0001) with CDCA-NCDs. Glycemic control, weight, and histopathology also favored CDCA-NCDs over free CDCA. Overall, CDCA-NCDs demonstrated excellent safety, efficient drug loading, controlled release, and superior therapeutic outcomes, supporting them as a promising low-frequency dosing strategy for neuroprotection and metabolic regulation in diabetic neuropathy. 30cm.

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