Neurodegenerative disorders and diseases (NDDs) that are either chronically acquired or triggered by a singular detrimental event are a rapidly growing cause of disability and/or death. In recent times, there have been major advancements in our understanding of various neurodegenerative disease states that have revealed common pathologic features or mechanisms. The many mechanistic parallels discovered between various neurodegenerative diseases suggest that a single therapeutic approach may be used to treat multiple disease conditions. Of late, natural compounds and supplemental substances have become an increasingly attractive option to treat NDDs because there is growing evidence that these nutritional constituents have potential adjunctive therapeutic effects (be it protective or restorative) on various neurodegenerative diseases. Here we review relevant experimental and clinical data on supplemental substances (i.e., curcuminoids, rosmarinic acid, resveratrol, acetyl-L-carnitine, and ω-3 (n-3) polyunsaturated fatty acids) that have demonstrated encouraging therapeutic effects on chronic diseases, such as Alzheimer's disease and neurodegeneration resulting from acute adverse events, such as traumatic brain injury.
Chronic spinal cord injury (SCI) often results in morbidity and mortality due to all-cause cardiovascular disease (CVD) and comorbid endocrine disorders. Several component risk factors for CVD, described as the (CMS), are prevalent in SCI, with the individual risks of obesity and insulin resistance known to advance the disease prognosis to a greater extent than other established risks. Notably, adiposity and insulin resistance are attributed in large part to a commonly observed maladaptive dietary/nutritional profile. Although there are no evidence-based nutritional guidelines to address the CMS risk in SCI, contemporary treatment strategies advocate more comprehensive lifestyle management that includes sustained nutritional guidance as a necessary component for overall health management. This monograph describes factors in SCI that contribute to CMS risks, the current nutritional profile and its contribution to CMS risks, and effective treatment strategies including the adaptability of the Diabetes Prevention Program (DPP) to SCI. Establishing appropriate nutritional guidelines and recommendations will play an important role in addressing the CMS risks in SCI and preserving optimal long-term health.
Hyperactivation of N-methyl-D-aspartate receptors (NRs) is associated with neuronal cell death induced by traumatic brain injury (TBI) and many neurodegenerative conditions. NR signaling efficiency is dependent on receptor localization in membrane raft microdomains. Recently, excitotoxicity has been linked to autophagy, but mechanisms governing signal transduction remain unclear. Here we have identified protein interactions between NR2B signaling intermediates and the autophagic protein Beclin-1 in membrane rafts of the normal rat cerebral cortex. Moderate TBI induced rapid recruitment and association of NR2B and pCaMKII to membrane rafts, and translocation of Beclin-1 out of membrane microdomains. Furthermore, TBI caused significant increases in expression of key autophagic proteins and morphological hallmarks of autophagy that were significantly attenuated by treatment with the NR2B antagonist Ro 25-6981. Thus, stimulation of autophagy by NR2B signaling may be regulated by redistribution of Beclin-1 in membrane rafts after TBI.
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