Abstract
The pathogenesis of Alzheimer’s disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain’s vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer’s disease. OS and Aβ are linked to each other because Aβ induces OS, and OS increases the Aβ deposition. Thus, the answer to the question “which comes first: the chicken or the egg?” remains extremely difficult. In any case, the evidence for the primary occurrence of oxidative stress in AD is attractive. Thus, evidence indicates that a long period of gradual oxidative damage accumulation precedes and results in the appearance of clinical and pathological AD symptoms, including Aβ deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. Moreover, oxidative stress plays a crucial role in the pathogenesis of many risk factors for AD. Alzheimer’s disease begins many years before its symptoms, and antioxidant treatment can be an important therapeutic target for attacking the disease.
Highlights
oxidative stress (OS) and Aβ are linked to each other because Aβ induces OS in vivo and in vitro [44,45,46], and OS increases the production of Aβ [47,48,49,50]
46], and OS increases the production of Aβ [47,48,49,50]
Evidence from in vitro studies showed increased oxidative stress-mediated by NF-kB in response to neurons exposed to Aβ; this increased oxidative stress resulted in the accumulation of lipid peroxides and neurodegeneration [92]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. One is β amyloid (Aβ), which accumulates abnormally in AD brain tissues and forms extracellular plaques known to induce synaptic alterations and neurodegeneration [5,6]. That considers Aβ to possess a crucial role in the pathogenesis of the disease [26,27,28,29,30] According to this theory, the accumulation and deposition of Aβ is responsible for Tau aggregation and, for the cognitive and mnemonic decline observed in AD patients [31]. Studies on transgenic mice carrying mutations in the gene for APP demonstrated the existence of soluble Aβ (sAβ) oligomers long before the deposition of β-amyloid, further supporting the hypothesis that, in particular conditions such as over-production, soluble Aβ aggregates exist in the human brain even in the absence of plaques.
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