Alzheimer's disease combination treatment.

Fessel, Jeffrey

doi:10.1016/j.neurobiolaging.2017.10.022

Cited by 18 publications

(11 citation statements)

References 5 publications

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“…AD is a prevalent neurodegenerative disease that leads to cognitive dysfunction and memory loss in affected individuals [ 131 , 132 ]. The pathophysiology of AD is closely associated with the generation of neurofibrillary tangles and accumulation of amyloid plaques, especially in the cerebral cortex and the hippocampus [ 133 , 134 ].…”

Section: S-persulfidation By H 2 S In the Cnsmentioning

confidence: 99%

Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation

Sun

Nie

et al. 2021

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: Hydrogen sulfide (H2S) and hydrogen polysulfides are recognized as important signaling molecules that are generated physiologically in the body, including the central nervous system (CNS). Studies have shown that these two molecules are involved in cytoprotection against oxidative stress and inflammatory response. In the brain system, H2S and polysulfides exert multiple functions in both health and diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington's disease (HD), memory decline, and glioma. Mechanistically, S-Persulfidation (also known as S-sulfuration or S-sulfhydration) of target proteins is believed to be a fundamental mechanism that underlies H2S-regulated signaling pathways. Cysteine S-Persulfidation is an important paradigm of post-translational protein modification in the process of H2S signaling. This model is established as a critical redox mechanism to regulate numerous biological functions, especially in H2S-mediated neuroprotection and neurogenesis. Although the current research of S-Persulfidation is still in its infancy, accumulative evidence suggests that protein S-Persulfidation may share similar characteristics with protein S-nitrosylation. In this review, we will provide a comprehensive insight into the S-Persulfidation biology of H2S and polysulfides in neurological ailments and presume potential avenues for therapeutic development in these disorders based on S-Persulfidation of target proteins.

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Section: S-persulfidation By H 2 S In the Cnsmentioning

confidence: 99%

Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation

Sun

Nie

et al. 2021

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“…Hence, acetylcholinesterase inhibitors are utilized for treatment to limit acetylcholine degradation, increasing the function of neural cells by increasing the concentration of acetylcholine (Sharma, 2019). Still, focusing on Aβ, pTau, or acetylcholine alone is unlikely in addressing the complete range of symptoms associated with neurological disease pathology (Fessel, 2018).…”

Section: Alzheimer's Disease Treatments Under Investigationmentioning

confidence: 99%

Cardiometabolic Modification of Amyloid Beta in Alzheimer’s Disease Pathology

Hefner

Baliga

Amphay

et al. 2021

Front. Aging Neurosci.

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In recent years, several studies have suggested that cardiometabolic disorders, such as diabetes, obesity, hypertension, and dyslipidemia, share strong connections with the onset of neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease (AD). However, establishing a definitive link between medical disorders with coincident pathophysiologies is difficult due to etiological heterogeneity and underlying comorbidities. For this reason, amyloid β (Aβ), a physiological peptide derived from the sequential proteolysis of amyloid precursor protein (APP), serves as a crucial link that bridges the gap between cardiometabolic and neurodegenerative disorders. Aβ normally regulates neuronal synaptic function and repair; however, the intracellular accumulation of Aβ within the brain has been observed to play a critical role in AD pathology. A portion of Aβ is believed to originate from the brain itself and can readily cross the blood-brain barrier, while the rest resides in peripheral tissues that express APP required for Aβ generation such as the liver, pancreas, kidney, spleen, skin, and lungs. Consequently, numerous organs contribute to the body pool of total circulating Aβ, which can accumulate in the brain and facilitate neurodegeneration. Although the accumulation of Aβ corresponds with the onset of neurodegenerative disorders, the direct function of periphery born Aβ in AD pathophysiology is currently unknown. This review will highlight the contributions of individual cardiometabolic diseases including cardiovascular disease (CVD), type 2 diabetes (T2D), obesity, and non-alcoholic fatty liver disease (NAFLD) in elevating concentrations of circulating Aβ within the brain, as well as discuss the comorbid association of Aβ with AD pathology.

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“…The World Health Organization reported that the number of patients with AD is 50 million currently; it is projected to increase to 152 million by 2050 and, due to improved human longevity, eventually become the major cause of death in the world [ 1 ]. Significant global social and economic resources have been invested to clarify the molecular mechanisms underlying the pathogenesis of AD, but effective strategies for its prevention and treatment are still lacking [ 2 , 3 ]. Furthermore, at present, physicians diagnose AD based on their clinical experience and a series of complex examinations [ 4 , 5 ], and there is also a lack of simple and effective methods to diagnose early-stage AD.…”

Section: Introductionmentioning

confidence: 99%

Screening and Identification of Potential Peripheral Blood Biomarkers for Alzheimer’s Disease Based on Bioinformatics Analysis

Wang

2020

Med Sci Monit

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Alzheimer's disease combination treatment.

Cited by 18 publications

References 5 publications

Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation

Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation

Cardiometabolic Modification of Amyloid Beta in Alzheimer’s Disease Pathology

Screening and Identification of Potential Peripheral Blood Biomarkers for Alzheimer’s Disease Based on Bioinformatics Analysis

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