Polyphenols are secondary metabolites of plants and play a potential role in the prevention and treatment of neurodegenerative diseases (NND) such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) due to their unique physiological functions such as acting as antioxidants, being anti-inflammatory, being neuroprotective, and promoting intestinal health. Since dietary polyphenols exist in plant foods in the form of glycosylation or esterification or are combined with polymers, they need to undergo extensive metabolism through phase I and phase II biotransformations by various intestinal enzymes, as well as metabolism by the intestinal microbiota before they can be fully absorbed. Polyphenols improve intestinal microbiota disorders by influencing the structure and function of intestinal microbiota, inducing beneficial bacteria to produce a variety of metabolites such as short-chain fatty acids (SCFAs), promoting the secretion of hormones and neurotransmitters, and playing an important role in the prevention and treatment of NND by affecting the microbe–gut–brain axis. We review the ways in which some polyphenols can change the composition of the intestinal microbiota and their metabolites in AD or PD animal models to exert the role of slowing down the progression of NND, aiming to provide evidence for the role of polyphenols in slowing the progression of NND via the microbiota–gut–brain (MGB) axis.

Coronary artery disease (CAD) is the result of atherosclerotic plaque development in the wall of the coronary arteries. The underlying mechanism involves atherosclerosis of the arteries of the heart which is a relatively complex process comprising several steps. In CAD, atherosclerosis induces functional and structural changes. The pathogenesis of CAD results from various changes in and interactions between multiple cell types in the artery walls; these changes mainly include endothelial cell (EC) dysfunction, vascular smooth muscle cell (SMC) alteration, lipid deposition and macrophage activation. Various blood markers associated with an increased risk for cardiovascular endpoints have been identified; however, few have yet been shown to have a diagnostic impact or important clinical implications that would affect patient management. Noncoding RNAs, especially microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), can be stable in plasma and other body fluids and could therefore serve as biomarkers for some diseases. Many studies have shown that some miRNAs and lncRNAs play key roles in heart and vascular development and in cardiac pathophysiology. Thus, we summarize here the latest research progress, focusing on the molecular mechanism of miRNAs and lncRNAs in CAD, with the intent of seeking new targets for the treatment of heart disease.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. AD is characterized by the production and aggregation of beta-amyloid (Aβ) peptides, hyperphosphorylated tau proteins that form neurofibrillary tangles (NFTs), and subsequent neuroinflammation, synaptic dysfunction, autophagy and oxidative stress. Non-coding RNAs (ncRNAs) can be used as potential therapeutic targets and biomarkers due to their vital regulatory roles in multiple biological processes involved in disease development. The involvement of ncRNAs in the pathogenesis of AD has been increasingly recognized. Here, we review the ncRNAs implicated in AD and elaborate on their main regulatory pathways, which might have contributions for discovering novel therapeutic targets and drugs for AD.

Alzheimer’s disease (AD) is a degenerative disease of the central nervous system that is the most common type of senile dementia. Ferroptosis is a new type of iron-dependent programmed cell death identified in recent years that is different from other cell death forms. Ferroptosis is induced by excessive accumulation of lipid peroxides and reactive oxygen species (ROS) in cells. In recent years, it has been found that ferroptosis plays an important role in the pathological process of AD. Iron dyshomeostasis contribute to senile plaques (SP) deposition and neurofibrillary tangles (NFTs). Iron metabolism imbalance in brain and the dysfunction of endogenous antioxidant systems including system Xc- and glutathione peroxidase (GPX) are closely related to the etiopathogenesis of AD. Dysfunction of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy induced ferroptosis can accelerates the pathological process of AD. In addition, NRF2, through regulating the expression of a considerable number of genes related to ferroptosis, including genes related to iron and glutathione metabolism, plays an important role in the development of AD. Here, we review the potential interaction between AD and ferroptosis and the major pathways regulating ferroptosis in AD. We also review the active natural and synthetic compounds such as iron chelators, lipid peroxidation inhibitors and antioxidants available to treat AD by alleviating iron dyshomeostasis and preventing ferroptosis in mice and cell models to provide valuable information for the future treatment and prevention of AD.

The pathological features of Alzheimer's disease (AD) include senile plaques induced by amyloid-β (Aβ) protein deposits, neurofibrillary tangles formed by aggregates of hyperphosphorylated tau proteins and neuronal cell loss in specific position within the brain. Recent observations have suggested the possibility of an association between AD and cellular prion protein (PrP C ) levels. PrP C is a high affinity receptor for oligomeric Aβ and is important for Aβ-induced neurotoxicity and thus plays a critical role in AD pathogenesis. The determination of the relationship between PrP C and AD and the characterization of PrP C binding to Aβ will facilitate the development of novel therapies for AD.