Alzheimer’s Disease (AD) is the most common type of dementia. The circadian system, which is controlled by the master clock in the Suprachiasmatic Nucleus (SCN) of the hypothalamus, is crucial for various physiological processes. Studies have shown that changes in the circadian rhythms can deteriorate neurodegenerative diseases. Changes in the SCN are associated with cognitive decline in AD. The cognitive impairments in AD, especially memory dysfunctions, may be related to Circadian Rhythm Disturbances (CRDs). Moreover, rhythmic expression of clock genes is disrupted in AD patients. There is a circadian pattern of inflammatory processes in AD, and dysregulation of core clock genes promotes neuroinflammation. The present narrative review addresses the intricate link between CRDs and AD, revisiting the relevant cellular and molecular mechanisms. The association between CRDs and AD highlights the need for further investigation of the underlying mechanisms.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that leads to a decline in cognitive function, including memory. The exact causes of AD are not fully understood, and to date no treatments are available that can stop the progression of this neurocognitive disorder. AD is associated with progressive loss of neurons, synaptic connectivity, and disruption of neuroplasticity in the brain. Neuroplasticity is the nervous system’s ability to adapt and recover in response to experiences, injuries, or a pathological change. Synaptic dysfunction and impairment of neuroplasticity are important elements of AD progression and cognitive decline. Studies have demonstrated that enhancement of neuroplasticity effectively improves cognition and memory, preventing the progression of AD. In this narrative review, we discuss the role of various pathophysiological explanations regarding the impairment of neuroplasticity in the pathogenesis of AD. We also highlight neuromodulation approaches, such as exercise, neurotrophic factor mimetics, pharmacological drugs, light therapy, and diet therapy that can promote neuroplasticity and have the potential for use in the prevention and treatment of AD.

Background and Aim: Spinal cord injury (SCI) leads to sensory, motor, and autonomic dysfunctions and changes in different nerve fibers that can greatly impact the quality of life of many people. Neuroplasticity is a spontaneous mechanism of the nervous system to adapt to different molecular, physiological, and anatomical changes after SCI. Methods and Materials/Patients: A literature search of relevant articles was made with a focus on recent publications. Results: This narrative review first discusses the definition of neuroplasticity in the nervous system and cellular processes of neuroplasticity in the synapses and their effects on synaptogenesis and neuroplasticity. We describe some of the important central and spinal neuronal pathways and their role in voluntary movements and the regenerative capacity in neuroplasticity and functional recovery. Then this review focuses on the effects of exercise and training programs and different neuromodulation techniques using electrical stimulation (ES) on the development of neuroplasticity. These rehabilitation and neuromodulation techniques accelerate the release of some neurotrophic factors to enhance neuroplasticity and functional sensorimotor recovery. Conclusion: This narrative review emphasizes the importance and capability of neuroplasticity in improving functional recovery and quality of life of the people following SCI. It identifies that different physical rehabilitation and neuromodulation strategies induce significant improvements in sensorimotor recovery and underlines that the combination of rehabilitation and neuromodulation techniques provides greater functional outcomes. There is a need for further investigation using preclinical and clinical studies in the future that should concentrate on the basic molecular and cellular processes of neuroplasticity and investment in enhancing the rehabilitation and neuromodulation techniques and finding new techniques.

Background The stress hyperglycemia is different from diabetes and is common after an acute illness such as stroke. Objective This study aimed to compare the effect of intravenous (IV) and subcutaneous (SQ) insulin injections on controlling hyperglycemia in diabetic patients with acute ischemic stroke (AIS). Methods This cross-sectional analytical study was conducted on 242 diabetic patients with AIS referred to the Emergency Department of Poursina Hospital in Rasht, Iran. During the treatment, the patients were subjected to SQ or IV insulin protocols. In each group, patients’ blood glucose and potassium levels in the first 24 hours, along with other variables, were recorded and compared between the two groups using independent t-test, chi-square test, or repeated measures analysis of variance. Results The mean blood glucose levels in the SQ insulin group at the time of admission and 6 and 12 hours after admission were significantly lower than in the IV insulin group. The blood sugar reduction, especially 6 hours after admission, was considerably higher in the IV insulin group. The incidence of hypokalemia in the IV insulin group was significantly higher than in the SQ insulin group. In almost all cases, IV insulin administration resulted in a faster and more effective reduction in blood sugar levels within 6 hours after admission compared to the SQ administration. Also, patients with higher initial blood levels responded significantly better to IV insulin protocol in reducing blood sugar levels. Conclusion The IV insulin protocol is more effective than the SQ insulin protocol in controlling or reducing hyperglycemia in diabetic patients with AIS in the first hours of admission and does not cause serious complications.