Search Results (3)

Background/aim: A growing body of evidence suggests a link between dyslipidemias and neurodegenerative diseases, highlighting the crucial role of lipid metabolism in the health of the central nervous system. The aim of our work was to provide an update on this topic, with a focus on clinical practice from an endocrinological point of view. Endocrinologists, being experts in the management of dyslipidemias, can play a key role in the prevention and treatment of neurodegenerative conditions, through precocious and effective lipid profile optimization. Methods: The literature was scanned to identify clinical trials and correlation studies on the association between dyslipidemia, statin therapy, and the following neurodegenerative diseases: Alzheimer’s disease (AD), Parkisons’s disease (PD), Multiple sclerosis (MS), and Amyotrophic lateral sclerosis (ALS). Results: Impaired lipid homeostasis, such as that frequently observed in patients affected by obesity and diabetes, is related to neurodegenerative diseases, such as AD, PD, and other cognitive deficits related to aging. AD and related dementias are now a real priority health problem. In the United States, there are approximately 7 million subjects aged 65 and older living with AD and related dementias, and this number is projected to grow to 12 million in the coming decades. Lipid-lowering therapy with statins is an effective strategy in reducing serum low-density lipoprotein cholesterol to normal range concentrations and, therefore, cardiovascular disease risk; moreover, statins have been reported to have a positive effect on neurodegenerative diseases. Conclusions: Several pieces of research have found inconsistent information following our review. There was no association between statin use and ALS incidence. More positive evidence has emerged regarding statin use and AD/PD. However, further large-scale prospective randomized control trials are required to properly understand this issue. Full article

Parkinson’s disease (PD) is a neurodegenerative condition in which degeneration mostly occurs in the dopamine (DA)-producing neurons within the substantia nigra in the midbrain. As a result, individuals with this condition suffer from progressively worsening motor impairment because of the resulting DA deficiency, along with an array of other symptoms that, over time, force them into a completely debilitating state. As an age-related disease, PD has only risen in prevalence over the years; thus, an emphasis has recently been placed on discovering a new treatment for this condition that is capable of attenuating its progression. The gut microbiota has become an area of intrigue among PD studies, as research into this topic has shown that imbalances in the gut microbiota (colloquially known as gut dysbiosis) seemingly promote the primary etiologic factors that have been found to be associated with PD and its pathologic progression. With this knowledge, research into PD treatment has begun to expand beyond synthetic pharmaceutical compounds, as a growing emphasis has been placed on studying plant-derived polyphenolic compounds, namely flavonoids, as a new potential therapeutic approach. Due to their capacity to promote a state of homeostasis in the gut microbiota and their long-standing history as powerful medicinal agents, flavonoids have begun to be looked at as promising therapeutic agents capable of attenuating several of the pathologic states seen amidst PD through indirect and direct means. This review article focuses on three flavonoids, specifically epigallocatechin-3-gallate, quercetin, and kaempferol, discussing the mechanisms through which these powerful flavonoids can potentially prevent gut dysbiosis, neuroinflammation, and other molecular mechanisms involved in the pathogenesis and progression of PD, while also exploring their real-world application and how issues of bioavailability and potential drug interactions can be circumvented or exploited. Full article

Clinical and research studies have suggested a link between Parkinson’s disease (PD) and alterations in the circadian clock. Drosophila melanogaster may represent a useful model to study the relationship between the circadian clock and PD. Apart from the conservation of many genes, cellular mechanisms, signaling pathways, and neuronal processes, Drosophila shows an organized central nervous system and well-characterized complex behavioral phenotypes. In fact, Drosophila has been successfully used in the dissection of the circadian system and as a model for neurodegenerative disorders, including PD. Here, we describe the fly circadian and dopaminergic systems and report recent studies which indicate the presence of circadian abnormalities in some fly PD genetic models. We discuss the use of Drosophila to investigate whether, in adults, the disruption of the circadian system might be causative of brain neurodegeneration. We also consider approaches using Drosophila, which might provide new information on the link between PD and the circadian clock. As a corollary, since PD develops its symptomatology over a large part of the organism’s lifespan and given the relatively short lifespan of fruit flies, we suggest that genetic models of PD could be used to perform lifelong screens for drug-modulators of general and/or circadian-related PD traits. Full article