Foodborne pathogens are one of the main concerns in public health, which can have a serious impact on community health and health care systems. Contamination of foods by bacterial pathogens (such as Staphylococcus aureus, Streptococci, Legionella pneumophila, Escherichia coli, Campylobacter jejuni and Salmonella typhimurium) results in human infection. A typical example is the current issue with Coronavirus, which has the potential for foodborne transmission and ruling out such concerns is often difficult. Although, the possible dissemination of such viruses via the food chain has been raised. Standard bacterial detection methods require several hours or even days to obtain the results, and the delay may result in food poisoning to eventuate. Conventional biochemical and microbiological tests are expensive, complex, time-consuming and not always reliable. Therefore, there are urgent demands to develop simple, cheap, quick, sensitive, specific and reliable tests for the detection of these pathogens in foods. Recent advances in smart materials, nanomaterials and biomolecular modeling have been a quantum leap in the development of biosensors in overcoming the limitations of a conventional standard laboratory assay. This research aimed to critically review bacteriophage-based biosensors, used for the detection of foodborne pathogens, as well as their trends, outcomes and challenges are discussed. The future perspective in the use of simple and cheap biosensors is in the development of lab-on-chips, and its availability in every household to test the quality of their food.

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by progressive cognitive decline and memory loss, imposing a significant burden on affected individuals and their families. Despite the recent promising progress in therapeutic approaches, more needs to be done to understand the intricate molecular mechanisms underlying the development and progression of AD. Growing evidence points to epigenetic changes as playing a pivotal role in the pathogenesis of the disease. The dynamic interplay between genetic and environmental factors influences the epigenetic landscape in AD, altering gene expression patterns associated with key pathological events associated with disease pathogenesis. To this end, epigenetic alterations not only impact the expression of genes implicated in AD pathogenesis but also contribute to the dysregulation of crucial cellular processes, including synaptic plasticity, neuroinflammation, and oxidative stress. Understanding the complex epigenetic mechanisms in AD provides new avenues for therapeutic interventions. This review comprehensively examines the role of DNA methylation and histone modifications in the context of AD. It aims to contribute to a deeper understanding of AD pathogenesis and facilitate the development of targeted therapeutic strategies.

Alzheimer’s disease (AD) is a common neurodegenerative disorder that affects the elderly. One of the key features of AD is the accumulation of reactive oxygen species (ROS), which leads to an overall increase in oxidative damage. The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a master regulator of the antioxidant response in cells. Under low ROS levels, Nrf2 is kept in the cytoplasm. However, an increase in ROS production leads to a translocation of Nrf2 into the nucleus, where it activates the transcription of several genes involved in the cells’ antioxidant response. Additionally, Nrf2 activation increases autophagy function. However, in AD, the accumulation of Aβ and tau reduces Nrf2 levels, decreasing the antioxidant response. The reduced Nrf2 levels contribute to the further accumulation of Aβ and tau by impairing their autophagy-mediated turnover. In this review, we discuss the overwhelming evidence indicating that genetic or pharmacological activation of Nrf2 is as a potential approach to mitigate AD pathology.

Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease represent some of the most prevalent neurodegenerative disorders afflicting millions of people worldwide. Unfortunately, there is a lack of efficacious treatments to cure or stop the progression of these disorders. While the causes of such a lack of therapies can be attributed to various reasons, the disappointing results of recent clinical trials suggest the need for novel and innovative approaches. Since its discovery, there has been a growing excitement around the potential for CRISPR-Cas9 mediated gene editing to identify novel mechanistic insights into disease pathogenesis and to mediate accurate gene therapy. To this end, the literature is rich with experiments aimed at generating novel models of these disorders and offering proof-of-concept studies in preclinical animal models validating the great potential and versatility of this gene-editing system. In this review, we provide an overview of how the CRISPR-Cas9 systems have been used in these neurodegenerative disorders.