Unraveling the therapeutic efficacy of resveratrol in Alzheimer’s disease: an umbrella review of systematic evidence

Azargoonjahromi, Ali; Abutalebian, Fatemeh

doi:10.1186/s12986-024-00792-1

Cited by 8 publications

(1 citation statement)

References 134 publications

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“…The pathological hallmarks of AD include amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs), such as tau protein tangles [ 4 ], cholinergic dysfunction [ 5 ], glial cell activation [ 6 ], mitochondrial dysfunction [ 7 ], vascular abnormalities [ 8 ], calcium homeostasis [ 9 ], oxidative stress [ 10 ], and synaptic dysfunction [ 11 ]. These elements are associated with the degeneration of neurons, impede cognitive function, and require extensive medical attention [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

The duality of amyloid-β: its role in normal and Alzheimer’s disease states

Azargoonjahromi

2024

Mol Brain

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Alzheimer’s disease (AD) is a degenerative neurological condition that gradually impairs cognitive abilities, disrupts memory retention, and impedes daily functioning by impacting the cells of the brain. A key characteristic of AD is the accumulation of amyloid-beta (Aβ) plaques, which play pivotal roles in disease progression. These plaques initiate a cascade of events including neuroinflammation, synaptic dysfunction, tau pathology, oxidative stress, impaired protein clearance, mitochondrial dysfunction, and disrupted calcium homeostasis. Aβ accumulation is also closely associated with other hallmark features of AD, underscoring its significance. Aβ is generated through cleavage of the amyloid precursor protein (APP) and plays a dual role depending on its processing pathway. The non-amyloidogenic pathway reduces Aβ production and has neuroprotective and anti-inflammatory effects, whereas the amyloidogenic pathway leads to the production of Aβ peptides, including Aβ40 and Aβ42, which contribute to neurodegeneration and toxic effects in AD. Understanding the multifaceted role of Aβ, particularly in AD, is crucial for developing effective therapeutic strategies that target Aβ metabolism, aggregation, and clearance with the aim of mitigating the detrimental consequences of the disease. This review aims to explore the mechanisms and functions of Aβ under normal and abnormal conditions, particularly in AD, by examining both its beneficial and detrimental effects.

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Section: Introductionmentioning

confidence: 99%

The duality of amyloid-β: its role in normal and Alzheimer’s disease states

Azargoonjahromi

2024

Mol Brain

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Design, Synthesis, and Invitro Pharmacological Evaluation of Novel Resveratrol Surrogate Molecules against Alzheimer's Disease

Subramanian,

Kumarasamy

et al. 2024

Chemistry & Biodiversity

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A series of resveratrol surrogate molecules were designed, synthesized and biologically evaluated for inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) along with anti‐oxidant activity as potential novel multifunctional agents against Alzheimer’s disease (AD). Six novel compounds were synthesized by reacting (E)‐4‐(3,5‐Dimethoxystyryl) aniline with benzaldehyde and some selected derivatives of benzaldehyde in the presence of ethanol and a few drops of glacial acetic acid which followed the general scheme involved in the formation of Schiff bases. The spectral analysis data including FT‐IR, 1H‐NMR, 13C‐NMR, and Mass spectroscopy results were found to be in good agreement with the newly synthesized compounds (Resveratrol Surrogate Molecules 1‐6). The synthesized compounds were evaluated for their dual cholinesterase inhibitory activities, cytotoxic effect, and anti‐oxidant potential. The results showed that compound RSM‐5 showed potent inhibitory activity against AChE and BChE. In, addition the cytotoxicity of the compound RSM5 is less and found to be within the desirable limit indicating the potential safety of RSM5. Also, it possesses substantial anti‐oxidant activity which qualifies RSM5 as an anti‐AD agent. Taken together, these findings demonstrate that the molecule RSM5 had the most multifunctional properties and could be a promising lead molecule for the future development of drugs for Alzheimer’s treatments.

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Clinical Insights on Caloric Restriction Mimetics for Mitigating Brain Aging and Related Neurodegeneration

Trisal,

Singh

2024

Cell Mol Neurobiol

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Aging, an inevitable physiological process leading to a progressive decline in bodily functions, has been an abundantly researched domain with studies attempting to slow it down and reduce its debilitating effects. Investigations into the cellular and molecular pathways associated with aging have allowed the formulation of therapeutic strategies. Of these, caloric restriction (CR) has been implicated for its role in promoting healthy aging by modulating key molecular targets like Insulin/IGF-1, mTOR, and sirtuins. However, CR requires dedication and commitment to a strict regimen which poses a difficulty in maintaining consistency. To maneuver around cumbersome diets, Caloric Restriction Mimetics (CRMs) have emerged as promising alternatives by mimicking the beneficial effects of CR. This review elucidates the molecular foundations enabling CRMs like rapamycin, metformin, resveratrol, spermidine, and many more to function as suitable anti-aging molecules. Moreover, it explores clinical trials (retrieved from the clinicaltrials.gov database) aimed at demonstrating the efficacy of CRMs as effective candidates against age-related neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.

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Unraveling the therapeutic efficacy of resveratrol in Alzheimer’s disease: an umbrella review of systematic evidence

Cited by 8 publications

References 134 publications

The duality of amyloid-β: its role in normal and Alzheimer’s disease states

The duality of amyloid-β: its role in normal and Alzheimer’s disease states

Design, Synthesis, and Invitro Pharmacological Evaluation of Novel Resveratrol Surrogate Molecules against Alzheimer's Disease

Clinical Insights on Caloric Restriction Mimetics for Mitigating Brain Aging and Related Neurodegeneration

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