Pharmacological potential of calorie restriction mimetics in mitigating brain aging.

Quality of life is strongly influenced by brain aging, which is closely associated with neurodegeneration. With brain aging, various changes occur at the cellular, tissue, and organ levels, such as loss of proteostasis; dysregulation of nutrient sensing; abnormalities in the functions of mitochondria; and changes in neurophysiology. These changes also affect cognitive capabilities and result in mild to severe cognitive impairment.

Inefficient maturation of disease-linked mutant forms of the KCC2 potassium-chloride cotransporter correlates with predicted pathogenicity.

The potassium-chloride cotransporter 2 (KCC2) is required for neuronal development, and KCC2 dysregulation is implicated in several neurodevelopmental disorders, including schizophrenia, autism, and epilepsy. A dozen mutations in the KCC2-encoding gene, SLC12A5, are associated with these disorders, but few are fully characterized. To this end, we examined KCC2 biogenesis in a HEK293 cell model.

Neuroinflammaging and the Immune Landscape: The Role of Autophagy and Senescence in Aging Brain.

Neuroinflammation is closely linked to aging, which damages the structure and function of the brain. It is caused by the intricate interactions of immune cells in the aged brain, such as the dysregulated glial cells and the dysfunctional astrocytes. Aging-associated chronic low inflammation, referred to as neuroinflammaging, shows an upregulated proinflammatory response.

Gut-brain axis and brain health: modulating neuroinflammation, cognitive decline, and neurodegeneration.

The microbiota-gut-brain axis is a pivotal medium of crosstalk between the central nervous system (CNS) and the gastrointestinal tract. It is an intricate network of synergistic molecular pathways that exert their effects far beyond their local vicinity and even affect the systemic functioning of the body. The current review explores the involvement of the gut-brain axis (GBA) in the functioning of the nervous system, with a special emphasis on the neurodegeneration, cognitive decline, and neuroinflammation that occur in Alzheimer's disease (AD) and Parkinson's disease (PD).

Protective Effects of Chlorogenic Acid Against Amyloid-Beta-Induced Oxidative Stress and Ion Transport Dysfunction in SH-SY5Y Cells.

Caloric restriction mimetics mimic the beneficial effects of dietary restriction approaches, such as caloric restriction approaches, without limiting the dietary intake. Chlorogenic acid (CGA) acts as a caloric restriction mimetic; however, its neuroprotective mechanisms remain ambiguous. Therefore, in this study, we aimed to elucidate the neuroprotective effects of CGA on SH-SY5Y cells treated with amyloid-beta (Aβ)1-42.

Caloric restriction mimetics improve gut microbiota: a promising neurotherapeutics approach for managing age-related neurodegenerative disorders.

The gut microbiota (GM) produces various molecules that regulate the physiological functionality of the brain through the gut-brain axis (GBA). Studies suggest that alteration in GBA may lead to the onset and progression of various neurological dysfunctions. Moreover, aging is one of the prominent causes that contribute to the alteration of GBA.