Abstract
Simple SummaryAlzheimer’s disease (AD) is the most common neurodegenerative disease, intensifying impairments in cognition, behavior, and memory. Histopathological AD variations include extracellular senile plaques’ formation, tangling of intracellular neurofibrils, and synaptic and neuronal loss in the brain. Multiple evidence directly indicates that oxidative stress participates in an early phase of AD before cytopathology. Oxidative stress plays a crucial role in activating and causing various cell signaling pathways that result in lesion formations of toxic substances, which advances the disease. Antioxidants are widely preferred to combat oxidative stress, and those derived from natural sources, which are often incorporated into dietary habits, can play an important role in delaying the onset as well as reducing the progression of AD. However, this approach has not been extensively explored yet. Moreover, a combination of antioxidants in conjugation with a nutrient-rich diet might be more effective in tackling AD pathogenesis. Thus, considering the above-stated fact, this comprehensive review aims to elaborate the basics of AD and antioxidants, including the vitality of antioxidants in AD. Moreover, this review may help researchers to develop effectively and potentially improved antioxidant therapeutic strategies for this disease as it also deals with the clinical trials in the stated field.Alzheimer’s disease (AD) rate is accelerating with the increasing aging of the world’s population. The World Health Organization (WHO) stated AD as a global health priority. According to the WHO report, around 82 million people in 2030 and 152 million in 2050 will develop dementia (AD contributes 60% to 70% of cases), considering the current scenario. AD is the most common neurodegenerative disease, intensifying impairments in cognition, behavior, and memory. Histopathological AD variations include extracellular senile plaques’ formation, tangling of intracellular neurofibrils, and synaptic and neuronal loss in the brain. Multiple evidence directly indicates that oxidative stress participates in an early phase of AD before cytopathology. Moreover, oxidative stress is induced by almost all misfolded protein lumps like α-synuclein, amyloid-β, and others. Oxidative stress plays a crucial role in activating and causing various cell signaling pathways that result in lesion formations of toxic substances, which foster the development of the disease. Antioxidants are widely preferred to combat oxidative stress, and those derived from natural sources, which are often incorporated into dietary habits, can play an important role in delaying the onset as well as reducing the progression of AD. However, this approach has not been extensively explored yet. Moreover, there has been growing evidence that a combination of antioxidants in conjugation with a nutrient-rich diet might be more effective in tackling AD pathogenesis. Thus, considering the above-stated fact, this comprehensive review aims to elaborate the basics of AD and antioxidants, including the vitality of antioxidants in AD. Moreover, this review may help researchers to develop effectively and potentially improved antioxidant therapeutic strategies for this disease as it also deals with the clinical trials in the stated field.
Highlights
According to the World Health Organization (WHO), around 50 million individuals worldwide suffer from dementia, with roughly 10 million new cases occurring each year [1]
The introduction of glutathione ethyl ester in transgenic mice featuring a high expression of sterol regulatory element-binding protein2 (SREBP-2) has been shown to prevent neuroinflammation and neuronal damage [114]
Another study reported that streptozotocin-induced tau hyperphosphorylation in the hippocampus was substantially reduced by silibinin [167]. Though these results indicate that silibinin may be a novel therapeutic agent for treating Alzheimer’s disease (AD), no clinical trials are on board
Summary
According to the World Health Organization (WHO), around 50 million individuals worldwide suffer from dementia, with roughly 10 million new cases occurring each year [1]. Aβ causes lipid peroxidation by interacting with the lipid membrane depending on the 4-HNE (4-hydroxynonenal) induced oxidation of cysteine residue, which leads to the interaction of this lipid peroxidation product with the membrane proteins specific to the brain and disrupts their structure and functionality. Such an escalation can be detrimental to the metabolic proteins of the brain. This activity of Aβ suggests the association between oxidative stress and Aβ deposition [7]. Nausea, vomiting, loss of appetite, increased frequency of bowel movements, headache, constipation, confusion, and dizziness
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