Bone remodelling is a complex and tightly regulated process. Disruption of bone remodelling skewing towards resorption will cause osteoporosis and increase the risk of fragility fracture. Honey is a natural product containing various bioactive ingredients with health benefits, especially polyphenols. Therefore, honey may be a novel dietary supplement to prevent osteoporosis. This review aims to summarize the current evidence on the effects of honey on bone health. The evidence reported so far indicates a skeletal-beneficial effect of honey in animal models of osteoporosis. However, the number of studies on humans is limited. Honey can protect the bone via its antioxidant and anti-inflammatory properties, primarily through its polyphenol content that acts upon several signalling pathways, leading to bone anabolic and antiresorptive effects. In conclusion, honey is a potential functional food for bone health, but the dose and the bioactive contents of honey need to be verified prior to its application in humans.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles. Recent evidence highlights autophagy as a pivotal mechanism in cellular homeostasis, mediating the clearance of misfolded proteins and damaged organelles. However, impaired autophagy contributes significantly to AD pathogenesis by disrupting proteostasis, exacerbating neuroinflammation, and promoting synaptic dysfunction. This review aims to scrutinize the intricate relationship between autophagy dysfunction and AD progression, explaining key pathways including macroautophagy, chaperone-mediated autophagy (CMA), and selective autophagy processes such as mitophagy and aggrephagy. This further extends the discussion beyond the central nervous system, evaluating the role of hepatic autophagy in Aβ clearance and systemic metabolic regulation. An understanding of autophagy’s involvement in AD pathology via various mechanisms could give rise to a novel therapeutic strategy targeting autophagic modulation to mitigate disease progression in the future.

Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, multiple sclerosis, and amyotrophic lateral sclerosis share converging mechanisms of neuronal dysfunction, including protein aggregation, oxidative stress, and chronic neuroinflammation. Glial cells, once considered passive supporters, are now recognized as central drivers of these processes, offering both pathogenic triggers and therapeutic opportunities. Yet, despite compelling preclinical evidence, the translation of glial-targeted therapies into clinical success has been limited. This review provides a critical synthesis of current knowledge by examining therapeutic strategies through the lens of their translational challenges and failures. This narrative review highlights how interspecies variability of glial phenotypes, shifting neuroprotective versus neurotoxic states, limited biomarker stratification, and delivery barriers have constrained trials, such as anti-triggering receptor expressed on myeloid cells 2 (anti-TREM2) antibodies in AD and glial cell line-derived neurotrophic factor (GDNF) in PD. By analyzing these obstacles across major neurodegenerative disorders, this review argue that the next stage of glial medicine requires precision approaches that integrate stage-specific phenotyping, biomarker-guided patient selection, and innovative delivery platforms. Understanding not only what has been tried but why translation has stalled is essential to chart a roadmap for effective, disease-modifying glial therapies in the aging brain.

Extensive knowledge related to medicinal characteristics of plants by living in forest or semi-forest habitats and close observations of indigenous communities have led to the discoveries of the genus Lepisanthes and its traditional uses. The genus Lepisanthes is a member of the Sapindaceae family and is found in various regions of the world. Six species of Lepisanthes such as L. alata, L. amoena, L. fruticosa, L. senegalensis, L. rubiginosa, and L. tetraphylla are widely utilized in traditional and folk medicinal systems. They have been used for centuries for the treatment of ailments or symptoms such as pain, dizziness, high fever, frequent passing of watery stool (diarrhea), abscess, and healing of cuts and wounds. Various methodological approaches, mainly in vitro studies, have been employed to further explore the roles of the genus Lepisanthes. The studies identified that the genus Lepisanthes exerts beneficial effects such as antioxidant, antimicrobial, antihyperglycemic, antimalarial, analgesic, and antidiarrheal. However, the summary of the available literature remains inconclusive. This review aims to comprehensively address the botany, traditional uses, phytochemistry, methods, and pharmacological properties of the six commonly used Lepisanthes species. Hence, our review provides a scientific consensus that may be essential in translating the pharmacological properties of the genus Lepisanthes into future novel cost-effective medicines.

Objective: To explore the effects of kelulut honey on bone structure and histomorphometry against glucocorticoid-induced osteoporosis. Methods: Thirty-five male rats were used (n = 7). Twenty-eight adrenalectomized rats were divided into four groups; each group was given normal saline 0.9% (negative control), calcium water (positive control), kelulut honey (200 mg/kg/day and 400 mg/kg/day, respectively) treatment, respectively. All of them were administered with intramuscular injection of dexamethasone (120 μg/kg/day) to induce osteoporosis. Seven sham operated rats were given vehicle palm olein 0.05 mL/100 g/day by intramuscular injection and 0.1 mL/kg/day orally. All the treatments were given daily for 2 month. Lipid peroxidation and oxidative stress enzymes were measured. In addition, bone structural and histomorphometry analyses were also conducted. Results: Two-month glucocorticoid treatment increased the level of malondialdehyde and decreased superoxide dismutase significantly. No significant changes were found in the activities of catalase and glutathion peroxidase. Bone volume/tissue volume and trabecular number were significantly reduced while trabecular separation of the femoral bones was increased which corresponded to the decreased number of osteoblast surface after two months of receiving glucocorticoid treatment. Kelulut honey treatment restored the level of superoxide dismutase and reduced malondialdehyde significantly (P<0.05). Moreover, kelulut honey increased bone volume/tissue volume, trabecular number and decreased trabecular separation significantly (P<0.05), which were further confirmed by increased osteoblast surface and decreased osteoclast surface number (P<0.05). Conclusions: Kelulut honey may have potential bone protective effect, and may be a prophylaxis against glucocorticoid-induced osteoporosis.

We examined the evidence for intermittent fasting (IF) as a preventative tool to influence β-amyloid in animal models of Alzheimer’s disease (AD). A Scopus, Ovid, PubMed, and Web of Science (WoS), search yielded 29 results using the keywords “amyloid beta”, “intermittent fasting”, “intermittent caloric restriction”, “alternate day fasting”, “modified alternate-day fasting”, “time-restricted feeding”, “Ramadan fast”, “intermittent calori* restriction”, “intermittent restrictive diet”, and “Alzheimer*”. Five research articles addressed directly the effects of intermittent fasting on β-amyloid levels in animal models of AD: alternate day fasting (ADF) and time-restricted feeding (TRF) methods were incorporated in these studies. The study designs were found to be heterogeneous. Variations in the levels of β-amyloid peptides or plaque in either the hippocampus, cortical areas, or both in animals following dietary intervention were observed as compared to the ad libitum group. Non-significant changes were observed in three studies, while two studies interestingly demonstrated amelioration and reduction in β-amyloid levels. Given the conflicting results obtained from this study, significant care has to be taken into consideration before the protocol can be applied as a preventative approach to treat Alzheimer’s disease. Longitudinal research is warranted to fully grasp how dietary habits can help alleviate the disease either through upstream or downstream of AD pathology.