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Alzheimers Dement

December 2024

School of Medical & Allied Sciences, K.R. Mangalam University, Gurugram, Haryana, India.

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Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and long-term disabilities in term neonates. Caffeine exerts anti-inflammatory effects and has been used in neonatal intensive care units in recent decades. In our neonatal rat model of hypoxic-ischemic (HI) brain injury, we demonstrated that a single daily dose of caffeine (40 mg/kg) for 3 days post-HI reduced brain tissue loss and microgliosis compared to the vehicle group.

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Age-related macular degeneration (AMD) is a chronic multifactorial degenerative eye disease and one of the leading causes of irreversible blindness worldwide. Despite extensive research, there is no consensus on the predominant pathological mechanism leading to photoreceptor death. AMD is associated with molecular and cellular disruptions that ultimately result in photoreceptor degeneration.

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Background: The global incidence of type 2 diabetes (T2D) is rapidly increasing, with retinopathy being its most common complication and a leading cause of preventable blindness. Although the precise mechanisms involved in the development of diabetic retinopathy (DR) are not fully understood, defective immunomodulation is a recognized key factor in its pathophysiology. Regulatory T cells (Treg) regulate inflammation and promote regeneration, and while they are known to have important anti-inflammatory and neuroprotective roles in other tissues, including central nervous system, their role in the diabetic retina remains largely unknown.

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Accumulating evidence indicates that inherited astrocyte dysfunction can be a primary trigger for epilepsy development; however, the available data are rather limited. In addition, astrocytes are considered as a perspective target for the design of novel and improvement of the existing antiepileptic therapy. Piracetam and related nootropic drugs are widely used in the therapy of various epileptic disorders, but detailed mechanisms of racetams action and, in particular, their effects on glial functions are poorly understood.

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