Kefir is a fermented beverage with renowned probiotics that coexist in symbiotic association with other microorganisms in kefir grains. This beverage consumption is associated with a wide array of nutraceutical benefits, including anti-inflammatory, anti-oxidative, anti-cancer, anti-microbial, anti-diabetic, anti-hypertensive, and anti-hypercholesterolemic effects. Moreover, kefir can be adapted into different substrates which allow the production of new functional beverages to provide product diversification. Being safe and inexpensive, there is an immense global interest in kefir’s nutritional potential. Due to their promising benefits, kefir and kefir-like products have a great prospect for commercialization. This manuscript reviews the therapeutic aspects of kefir to date, and potential applications of kefir products in the health and food industries, along with the limitations. The literature reviewed here demonstrates that there is a growing demand for kefir as a functional food owing to a number of health-promoting properties.

Transient receptor potential melastatin 2 (TRPM2) proteins form Ca2+-permeable cationic channels that are potently activated by reactive oxygen species (ROS). ROS are produced during immune responses as signaling molecules as well as anti-microbial agents. ROS-sensitive TRPM2 channels are widely expressed in cells of the immune system and located on the cell surface as a Ca2+ influx pathway in macrophages, monocytes, neutrophils, lymphocytes and microglia but preferentially within the lysosomal membranes as a Ca2+ release mechanism in dendritic cells; ROS activation of the TRPM2 channels, regardless of the subcellular location, results in an increase in the intracellular Ca2+ concentrations. Recent studies have revealed that TRPM2-mediated ROS-sensitive Ca2+ signaling mechanisms play a crucial role in a number of processes and functions in immune cells. This mini-review discusses the recent advances in revelation of the various roles the TRPM2 channels have in immune cell functions and the implications in inflammatory diseases.

Excessive Zn²⁺ causes brain damage via promoting ROS generation. Here we investigated the role of ROS-sensitive TRPM2 channel in H₂O₂/Zn²⁺-induced Ca²⁺ signalling and cell death in microglial cells. H₂O₂/Zn²⁺ induced concentration-dependent increases in cytosolic Ca²⁺ concentration ([Ca²⁺]_c), which was inhibited by PJ34, a PARP inhibitor, and abolished by TRPM2 knockout (TRPM2-KO). Pathological concentrations of H₂O₂/Zn²⁺ induced substantial cell death that was inhibited by PJ34 and DPQ, PARP inhibitors, 2-APB, a TRPM2 channel inhibitor, and prevented by TRPM2-KO. Further analysis indicate that Zn²⁺ induced ROS production, PARP-1 stimulation, increase in the [Ca²⁺]_c and cell death, all of which were suppressed by chelerythrine, a protein kinase C inhibitor, DPI, a NADPH-dependent oxidase (NOX) inhibitor, GKT137831, a NOX1/4 inhibitor, and Phox-I2, a NOX2 inhibitor. Furthermore, Zn²⁺-induced PARP-1 stimulation, increase in the [Ca²⁺]_c and cell death were inhibited by PF431396, a Ca²⁺-sensitive PYK2 inhibitor, and U0126, a MEK/ERK inhibitor. Taken together, our study shows PKC/NOX-mediated ROS generation and PARP-1 activation as an important mechanism in Zn²⁺-induced TRPM2 channel activation and, TRPM2-mediated increase in the [Ca²⁺]_c to trigger the PYK2/MEK/ERK signalling pathway as a positive feedback mechanism that amplifies the TRPM2 channel activation. Activation of these TRPM2-depenent signalling mechanisms ultimately drives Zn²⁺-induced Ca²⁺ overloading and cell death.

The focus on managing Alzheimer’s disease (AD) is shifting towards prevention through lifestyle modification instead of treatments since the currently available treatment options are only capable of providing symptomatic relief marginally and result in various side effects. Numerous studies have reported that the intake of fermented foods resulted in the successful management of AD. Food fermentation is a biochemical process where the microorganisms metabolize the constituents of raw food materials, giving vastly different organoleptic properties and additional nutritional value, and improved biosafety effects in the final products. The consumption of fermented foods is associated with a wide array of nutraceutical benefits, including anti-oxidative, anti-inflammatory, neuroprotective, anti-apoptotic, anti-cancer, anti-fungal, anti-bacterial, immunomodulatory, and hypocholesterolemic properties. Due to their promising health benefits, fermented food products have a great prospect for commercialization in the food industry. This paper reviews the memory and cognitive enhancement and neuroprotective potential of fermented food products on AD, the recently commercialized fermented food products in the health and food industries, and their limitations. The literature reviewed here demonstrates a growing demand for fermented food products as alternative therapeutic options for the prevention and management of AD.

Alzheimer's disease (AD), an age-related neurodegenerative condition, is the most common cause of dementia among the elder people, but currently there is no treatment. A number of putative pathogenic events, particularly amyloid β peptide (Aβ) accumulation, are believed to be early triggers that initiate AD. However, thus far targeting Aβ generation/aggregation as the mainstay strategy of drug development has not led to effective AD-modifying therapeutics. Oxidative damage is a conspicuous feature of AD, but this remains poorly defined phenomenon and mechanistically ill understood. The TRPM2 channel has emerged as a potentially ubiquitous molecular mechanism mediating oxidative damage and thus plays a vital role in the pathogenesis and progression of diverse neurodegenerative diseases. This article will review the emerging evidence from recent studies and propose a novel 'hypothesis' that multiple TRPM2-mediated cellular and molecular mechanisms cascade Aβ and/or oxidative damage to AD pathologies. The 'hypothesis' based on these new findings discusses the prospect of considering the TRPM2 channel as a novel therapeutic target for intervening AD and age-related dementia.