Prader-Willi syndrome (PWS) is a rare genetic disorder due to lack of genes expression inherited from the paternal chromosome 15q11-q13 region usually from paternal deletions, maternal uniparental disomy 15 or imprinting defect. There are two different nutritional stages reported in an individual with PWS; first stage during infancy marked by feeding and growth difficulties and second stage where hyperphagia starts and leads to development of obesity. However, the exact mechanism of hyperphagia development, from having difficulties in feeding during early years to insatiable appetite after they grow is still unknown and is the focused in this review. The keywords used for literature search such as "Prader-Willi syndrome", "hyperphagia", "obesity", and "treatment" were used to create the search strings by using synonyms in order to retrieve the relevant records from PubMed, Scopus and Science Direct. The possible mechanism of hyperphagia can be classed into hormonal abnormalities such as increase in ghrelin and leptin from infancy to adulthood. Low level of hormones was observed in the thyroid, insulin and peptide YY at certain ages. Neuronal abnormalities contributed by Orexin A and brain structure alteration was documented at 4-30 years old. Treatment in the form of drugs such as livoletide, topiramate, and diazoxide could potentially alleviate these abnormalities and make hyperphagia less prominent in PWS. The approaches are important to regulate the hormonal changes and neuronal involvement as potentially controlling hyperphagia and obesity.

Lysosome is a primary degradative organelle and is crucial in cellular homeostasis. A reduction in its function due to ageing has been associated with the development of Alzheimer's disease (AD), a common neurodegenerative disorder characterised by the deposition of neurotoxic amyloid plaque in the brain and cerebral vessel walls. The breakdown of the blood-brain barrier (BBB) plays a vital role in the pathogenesis of AD. However, the impact of lysosomal dysfunction on brain endothelial cells, the key component of the BBB, in the disease progression is yet to be fully understood. In this study, human brain endothelial cells (HBEC-5i) were exposed to a lysosomotropic compound, chloroquine (CQ) for 24 h. Cell viability was assessed with the 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay to determine the inhibitory concentration (IC) at IC₁₀ (17.5 µM), IC₂₅ (70.5 µM), and IC₅₀ (125 µM). The morphological changes observed include vacuoles arrested in the cytosols and cell shrinkage that were more prominent at IC₂₅ and IC₅₀. Lysosomal dysfunction was evaluated by measuring the lysosomal-associated membrane protein-1 (LAMP-1) and microtubule-associated protein light chain 3-II (LC3-II) using the capillary-based immunoassay. LC3-II was significantly increased at IC₂₅ and IC₅₀ (p < 0.05 and p < 0.001_, respectively). The concentration of intracellular and extracellular Aβ42 was quantitated using the enzyme-linked immunosorbent assay, which demonstrated a significant increase (p < 0.05) in intracellular Aβ42 at IC₂₅. This study showed that perturbation of lysosomal function impairs autophagy that leads to intracellular increment of Aβ, indicating the important roles of lysosomes in endothelial cells homeostasis and disease progression.

Coronary artery disease (CAD) accelerates cardiovascular morbidity and complications that threaten public health, necessitating a deeper understanding of its molecular regulators. This systematic review synthesizes evidence on long noncoding RNA (lncMALAT1), a critical indicator of CAD progression through the regulation of autophagy, apoptosis, inflammation, and vascular remodeling. Analyzing 23 experimental studies (PRISMA-guided, PROSPERO-registered), we have identified key findings including MALAT1 modulation altered cardiac function, microstructure via miRNAs-mediated- pathways through in-vivo studies. In-vitro studies emphasized overexpression, knockdown, and combined both approaches. These studies investigated potential molecular targets and biological changes, while emphasizing miRNAs. Hypoxia or hypoxia/reoxygenation conditions were explored, revealing insights into apoptosis and cell viability. Innovations include mapping MALAT1’s interaction networks across both in-vivo and in-vitro experimental CAD contexts. The findings synthesized the role of lncMALAT1 in CAD, highlighting its potential as a biomarker and therapeutic target. Future research should focus on standardizing experimental designs and elucidating precise mechanisms.

The brain plays a central role in controlling and regulating bodily activities. Given its significance, the brain needs to remain in optimal condition to function properly. Neurodegenerative diseases arise when the mechanisms maintaining brain homeostasis fail, resulting in prolonged and uncontrolled activation of cell death pathways. Increasingly, researchers are focusing on specific types of cell death, such as ferroptosis and pyroptosis, due to their potential as targets for preventing and treating neurodegenerative diseases. Brain-derived neurotrophic factor (BDNF) is a crucial growth factor for neurogenesis, neuronal survival, and maintenance, and is thus implicated in cell death mechanisms. This review aims to elucidate the role of BDNF in the ferroptosis and pyroptosis mechanisms that impact brain health. To achieve this, three databases – PubMed, Scopus, and Web of Science – were searched for relevant studies, yielding 95 articles, of which only 14 were aligned with the study’s aim. Ferroptosis (iron-dependent cell death) and pyroptosis (inflammatory cell death) are distinct modes of cell death; however, this review found both mechanisms are associated with oxidative stress. Consequently, the findings suggest that ferroptosis and pyroptosis collectively impact brain health conditions such as depression, cognitive deficiencies, and anxiety, which are notably linked to reduced BDNF levels.

1. Coronary artery disease (CAD) remains a leading cause of morbidity and mortality worldwide, accounting for approximately 25% of all-cause deaths annually [1]. Despite advances in cardiovascular ...