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Abstract Alzheimer's disease (AD) is considered to be the most typical form of dementia that provokes irreversible cognitive impairment. Along with cognitive impairment, circadian rhythm dysfunction is a fundamental factor in aggravating AD. A link among circadian rhythms, sleep, and AD has been well‐documented. The etiopathogenesis of circadian system disruptions and AD serves some general characteristics that also open up the possibility of viewing them as a mutually reliant path. In this review, we have focused on different factors that are related to circadian rhythm dysfunction. The various pathogenic factors, such as amyloid‐beta, neurofibrillary tangles, oxidative stress, neuroinflammation, and circadian rhythm dysfunction may all contribute to AD. In this review, we also tried to focus on melatonin which is produced from the pineal gland and can be used to treat circadian dysfunction in AD. Aside from amyloid beta, tau pathology may have a notable influence on sleep. Conclusively, the center of this review is primarily based on the principal mechanistic complexities associated with circadian rhythm disruption, sleep deprivation, and AD, and it also emphasizes the potential therapeutic strategies to treat and prevent the progression of AD.

Alzheimer's disease (AD) is considered to be the most typical form of dementia that provokes irreversible cognitive impairment. Along with cognitive impairment, circadian rhythm dysfunction is a fundamental factor in aggravating AD. A link among circadian rhythms, sleep, and AD has been well‐documented. The etiopathogenesis of circadian system disruptions and AD serves some general characteristics that also open up the possibility of viewing them as a mutually reliant path. In this review, we have focused on different factors that are related to circadian rhythm dysfunction. The various pathogenic factors, such as amyloid‐beta, neurofibrillary tangles, oxidative stress, neuroinflammation, and circadian rhythm dysfunction may all contribute to AD. In this review, we also tried to focus on melatonin which is produced from the pineal gland and can be used to treat circadian dysfunction in AD. Aside from amyloid beta, tau pathology may have a notable influence on sleep. Conclusively, the center of this review is primarily based on the principal mechanistic complexities associated with circadian rhythm disruption, sleep deprivation, and AD, and it also emphasizes the potential therapeutic strategies to treat and prevent the progression of AD. [ABSTRACT FROM AUTHOR]

The Ethics Subcommittee of AMDA–The Society for Post-Acute and Long-Term Care Medicine ("The Society") presents arguments for and against Stopping Eating and Drinking by Advance Directives (SED by AD). SED by AD is a type of advance directive in which a proxy is instructed to stop offering food and fluids to a person when they reach a certain stage of dementia. Although most conversations regarding SED by AD focus on patient autonomy and the right to determine one's care, we propose that the ethical principle of justice—the obligation to treat all individuals equally regardless of race, gender, and physical or cognitive ability—is the decisive principle in this controversy. We also suggest that implementing SED by AD can violate a physician's obligation to beneficence and nonmaleficence. On the other hand, we identify with the families of our patients who see the refusal to follow an advance directive as an injustice of the highest order. In the end, The Society is convinced that no choice can be made here without practicing an injustice: if one refuses to implement SED by AD, one violates the autonomy of the person who drew up the advance directive. If, on the other hand, one refuses food and fluid to a resident who still accepts food, one risks practicing an injustice against that person as they are now. Recognizing that we have the greatest responsibility to our patients as they present to us in the residential setting, The Society recommends against implementing SED by AD in residents who still accept food and fluids, implementing instead, a policy of comfort feeding for those with advanced dementia. [ABSTRACT FROM AUTHOR]

Transgenic Drosophila melanogaster lines modeling the main neuromorphological markers of Alzheimer's disease were used to study the neuroprotective properties of nicotinic acid. Thirty days old flies treated with nicotinic acid showed better survival rate and reduced neurodegeneration.

Because of the complex cascade of molecular events that can occur in the brain of an Alzheimer''s disease (AD) patient, the therapy of this neurodegenerative disease seems more likely to be achieved by multifunctional drugs. Herein, a new series of dual-targeting ligands have been developed and in vitro bioevaluated. Their architecture is based on conjugating the acetylcholinesterase inhibition and anti-oxidant properties in one molecular entity. Specifically, a series of naturally occurring phenolic acids with recognized anti-oxidant properties (derivatives of caffeic acid, rosmarinic acid, and trolox) have been conjugated with choline to account for the recognition by acetylcholinesterase (AChE). The synthesized hybrid compounds evidenced AChE inhibitory capacity of micromolar range (rationalized by molecular modeling studies) and good antioxidant properties. Their effects on human neuroblastoma cells, previously treated with beta-amyloid peptides and 1-methyl-4-phenylpyridinium ion neurotoxins (to simulate AD and Parkinson''s disease, respectively), also demonstrated a considerable capacity for protection against the cytotoxicity of these stressors. [ABSTRACT FROM AUTHOR]

Current interest in amyloid fibrils stems from their involvement in neurodegenerative and other diseases and from their role as an alternative structural state for many peptides and proteins. Solid-state nuclear magnetic resonance (NMR) methods have the unique capability of providing detailed structural constraints for amyloid fibrils, sufficient for the development of full molecular models. In this article, recent progress in the application of solid-state NMR to fibrils associated with Alzheimer's disease, prion fibrils, and related systems is reviewed, along with relevant developments in solid-state NMR techniques and technology. [ABSTRACT FROM AUTHOR]

Objectives: Estrogen is known to prominently benefit neuronal syndromes and neurodegenerative diseases. Ginsenoside Rg1, an active ingredient found in a Chinese plant, ginseng root, was previously demonstrated to exert estrogen-like activity. This study was performed to assess the neuroprotective effect of ginsenoside Rg1 against apoptosis induced by ββ-amyloid protein 25--35 (Aββ25--35) in primary cultured rat hippocampal neuronal cells as well as in the underlying mechanisms. Methods: We first measured cell viability and lactate dehydrogenase (LDH) release from primary cultured rat hippocampal neurons. After that, the inhibition effects of ginsenoside Rg1 on neuronal cell apoptosis were evaluated with flow cytometric analysis. Furthermore, western blot analysis was used for detecting the expression of apoptosis-related proteins Bcl-2, Bax, and active caspase 3. Results: The results show that ginsenoside Rg1 could increase neuronal viability and reduce LDH release; rescue cell apoptosis induced by Aββ25--35; decrease the expression of caspase 3, increase the ratio of Bcl-2/Bax at the protein levels compared with the cells only treated with Aββ25--35. Conclusions: Taken together, our results indicate that the apoptosis induced by Aββ25--35 could be reversed by ginsenoside Rg1. Furthermore, this neuroprotective effect is probably mediated by up-regulating the ratio of Bcl-2/Bax that activates caspase 3. [ABSTRACT FROM AUTHOR]