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• Organic acids are acid in nature. • Dietary organic acids have no risk factors. • Organic acids have antimicrobial activity. • They attenuate Alzheimer disease via antioxidant activity to affect the amyloid aggregation pathway. Organic acids are specific groups of chemicals that contain COOH in their structures. They have properties of weakly acidic nature and dissolves completely into protons when present in aqueous solutions. In biological systems, organic acids are involved in various activities such as important intermediates in various metabolic cycles, antimicrobial compounds, and prediction of maturity indices. Due to these properties, organic acids are important phytochemicals that have a wide range of commercial applications like animal feeds utilization, improve plant quality, bactericidal and bacteriostatic potential, as well as in the pharmaceutical industry for numerous preparations. In pharmacokinetics, organic acids are primarily involved in the absorption of pH-dependent drugs. Different techniques have been employed for the extraction, purification, and quantification of organic acids. Among them, microwave-assisted extractions (MAE) and ultrasound-assisted extractions (UAE) are the chiefly used techniques where MAE is one of the most valuable methods for isolating different compounds from plant materials for industrial and analytical purposes. Moreover, bioactive chemicals such as natural organic acid from plants and other sources are important and referred as "lifespan essential"since they havea beneficial effect on healthy aging and Alzheimer's disease (AD). Therefore, dietary organic acids and avoiding risk factors, will reduce the risk of neurodegenerative diseases such as AD and increase a healthy lifespan. Thus, the present study aimed to understand the phytochemistry, biological activities, industrial applications, possible interaction with other drugs/foods supplements,techniques of extraction, purification and fractionation, techniques of identification and quantification, the effect of food processing,and molecular mechanisms of organic acid to attenuate AD. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer's pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis. [ABSTRACT FROM AUTHOR]

Quercetin belongs to the flavonoids family, which is present in most of the plants including fruits, vegetables, green tea and even in red wine having antioxidant activities. It is available as a food supplement in the market and has physiological health effects. Quercetin has anti-inflammatory, anticancer and anti-prostate activities along with its beneficial effects on high cholesterol, kidney transplantation, asthma, diabetes, viral infections, pulmonary, schizophrenia and cardiovascular diseases. Quercetin possesses scavenging potential of hydroxyl radical (OH−), hydrogen peroxide (H 2 O 2), and superoxide anion (O 2 −). These reactive oxygen species (ROS) hampers lipid, protein, amino acids and deoxyribonucleic acid (DNA) processing leading to epigenetic alterations. Quercetin has the ability to combat these harmful effects. ROS plays a vital role in the progression of Alzheimer's disease (AD), and we propose that quercetin would be the best choice to overcome cellular and molecular signals in regulating normal physiological functions. However, data are not well documented regarding exact cellular mechanisms of quercetin. The neuroprotective effects of quercetin are mainly due to potential up- and/or down-regulation of cytokines via nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Paraoxonase-2, c-Jun N-terminal kinase (JNK), Protein kinase C, Mitogen-activated protein kinase (MAPK) signalling cascades, and PI3K/Akt pathways. Therefore, the aim of the present review was to elaborate on the cellular and molecular mechanisms of the quercetin involved in the protection against AD. Unlabelled Image • Quercetin improves cellular functions. • Quercetin acts via modulating signalling pathways and gene expressions. • Quercetin-induced Nrf-2 translocation from the cytoplasm to the nucleus • Quercetin ameliorates AD via antioxidant pathways. [ABSTRACT FROM AUTHOR]

• Sleep deprivation and circadian dysfunction are both present in Alzheimer's disease. • Evidence suggests a bidirectional relationship between circadian rhythms, sleep, and Alzheimer's disease. • Complex impacts of circadian dysfunction, neuroinflammation, and oxidative stress are operative in Alzheimer's pathology. • Loss of melatonin is becoming a hallmark of Alzheimer's disease and its supplementation induces better sleep time in Alzheimer's patients. Alzheimer's disease (AD) is a devastating and irreversible cognitive impairment and the most common type of dementia. Along with progressive cognitive impairment, dysfunction of the circadian rhythms also plays a pivotal role in the progression of AD. A mutual relationship among circadian rhythms, sleep, and AD has been well-recommended. The etiopathogenesis of the disturbances of the circadian system and AD share some general features that also unlock the outlook of observing them as a mutually dependent pathway. Indeed, the burden of amyloid β (Aβ), neurofibrillary tangles (NFTs), neuroinflammation, oxidative stress, and dysfunction of circadian rhythms may lead to AD. Aging can alter both sleep timings and quality that can be strongly disrupted in AD. Increased production of Aβ and reduced Aβ clearance are caused by a close interplay of Aβ, sleep disturbance and raised wakefulness. Besides Aβ, the impact of tau pathology is possibly noteworthy to the sleep deprivation found in AD. Hence, this review is focused on the primary mechanistic complexities linked to disruption of circadian rhythms, sleep deprivation, and AD. Furthermore, this review also highlights the potential therapeutic strategies to abate AD pathogenesis. [ABSTRACT FROM AUTHOR]