Even though Alzheimer’s disease (AD) is of significant interest to the scientific community, its pathogenesis is very complicated and not well-understood. A great deal of progress has been made in AD research recently and with the advent of these new insights more therapeutic benefits may be identified that could help patients around the world. Much of the research in AD thus far has been very neuron-oriented; however, recent studies suggest that glial cells, i.e., microglia, astrocytes, oligodendrocytes, and oligodendrocyte progenitor cells (NG2 glia), are linked to the pathogenesis of AD and may offer several potential therapeutic targets against AD. In addition to a number of other functions, glial cells are responsible for maintaining homeostasis (i.e., concentration of ions, neurotransmitters, etc.) within the central nervous system (CNS) and are crucial to the structural integrity of neurons. This review explores the: (i) role of glial cells in AD pathogenesis; (ii) complex functionalities of the components involved; and (iii) potential therapeutic targets that could eventually lead to a better quality of life for AD patients.

Childhood obesity accounts for several psychosocial and clinical consequences. Psychosocial consequences include lower self-esteem, social isolation, poor academic achievement, peer problems, and depression, whereas clinical consequences are cardiovascular diseases, type 2 diabetes, dyslipidemia, cancer, autoimmune diseases, girls early polycystic ovarian syndrome (PCOS), asthma, bone deformities, etc. A growing number of studies have uncovered the association of childhood obesity and its consequences with vitamin-D (vit-D) deficiency and vitamin-D receptor (VDR) gene polymorphisms such as single nucleotide polymorphisms (SNPs), e.g., TaqI, BsmI, ApaI, FokI, and Cdx2. Considering the impact of vit-D deficiency and VDR gene polymorphisms, identifying associated factors and risk groups linked to lower serum vit-D levels and prevention of obesity-related syndromes in children is of utmost importance. Previously published review articles mainly focused on the association of vit-D deficiency with obesity or other non-communicable diseases in children. The nature of the correlation between vit-D deficiency and VDR gene polymorphisms with obesity in children is yet to be clarified. Therefore, this review attempts to delineate the association of obesity with these two factors by identifying the molecular mechanism of the relationship.

Objective To recruit South Asian pregnant women, living in the UK, into a clinicoepidemiological study for the collection of lifestyle survey data and antenatal blood and to retain the women for the later collection of cord blood and meconium samples from their babies for biochemical analysis. Design A longitudinal study recruiting pregnant women of South Asian and Caucasian origin living in the UK. Setting Recruitment of the participants, collection of clinical samples and survey data took place at the 2 sites within a single UK Northern Hospital Trust. Participants Pregnant women of South Asian origin (study group, n=98) and of Caucasian origin (comparison group, n=38) living in Leeds, UK. Results Among the participants approached, 81% agreed to take part in the study while a ‘direct approach’ method was followed. The retention rate of the participants was a remarkable 93.4%. The main challenges in recruiting the ethnic minority participants were their cultural and religious conservativeness, language barrier, lack of interest and feeling of extra ‘stress’ in taking part in research. The chief investigator developed an innovative participant retention method, associated with the women's cultural and religious practices. The method proved useful in retaining the participants for about 5 months and in enabling successful collection of clinical samples from the same mother–baby pairs. The collection of clinical samples and lifestyle data exceeded the calculated sample size required to give the study sufficient power. The numbers of samples obtained were: maternal blood (n=171), cord blood (n=38), meconium (n=176), lifestyle questionnaire data (n=136) and postnatal records (n=136). Conclusions Recruitment and retention of participants, according to the calculated sample size, ensured sufficient power and success for a clinicoepidemiological study. Results suggest that development of trust and confidence between the participant and the researcher is the key to the success of a clinical and epidemiological study involving ethnic minorities.

The online version contains supplementary material available at 10.1038/s41598-026-39794-9.

Recently, some researchers claimed neuropathological changes lead to Alzheimer’s-like brains after severe infection of SARS-CoV-2. Several mechanisms have been postulated on how SARS-CoV-2 neurological damage leads to Alzheimer's disease (AD) development. Neurobiochemical changes during infection may significantly induce Alzheimer's disease in severely COVID-19 infected people. The immune system is also compromised while infected by this novel coronavirus. However, recent studies are insufficient to conclude the relationship between Alzheimer's disease and COVID-19. This review demonstrates the possible pathways of neuropathological changes induced by the SARS-CoV-2 virus in AD patients or leading to AD in COVID-19 patients. Therefore, this study delineates the challenges for COVID-19 infected AD patients and the mechanism of actions of natural compounds and alternative treatments to overcome those. Furthermore, animal studies and a large cohort of COVID-19 survivors who showed neuroinflammation and neurological changes may augment the research to discover the relationship between Alzheimer's disease and COVID-19.