Alzheimer’s Disease: The Past, Present, and Future of a Globally Progressive Disease

Abstract

Alzheimer’s disease (AD) is a significant 21st-century public health challenge. This article delves into AD's neurodegenerative complexities, highlighting cognitive decline, memory impairment, and societal burdens. Mechanistically, protein misfolding, amyloid-beta (Aβ) pathway abnormalities, and genetic/environmental factors are discussed. The pivotal amyloid hypothesis is dissected, focusing on Aβ aggregation's role in synaptic dysfunction and neurodegeneration. The review showcases promising therapeutic strategies, including anti-amyloid antibodies and β/γ-secretase inhibitors targeting Aβ production. Notably, the FDA-approved Lecanemab signifies a breakthrough, slowing disease progression. Anti-Tau therapies' emergence is highlighted, addressing late-stage intervention. Tau aggregation blockers and anti-Tau antibodies offer potential against intracellular tau pathology. The review underscores collaborative efforts to uncover AD's secrets and pave the way for memory preservation.

Exploring the Role of Apigenin in Neuroinflammation: Insights and Implications

“…Neuronal degeneration first affects neurons in the hippocampus, leading to impairment of short-term memory, and then gradually spreads throughout the brain. Two proteins are involved: (1) amyloid beta peptide, which accumulates abnormally, forming plaques known as amyloid plaques or "senile" plaques (this accumulation is toxic to nerve cells in affected patients) and (2) tau protein, which is altered in affected patients, causing successive disorganization of neurons, accumulation of filaments inside them (neurofibrillary degeneration), and then nerve cell death [92]. Degeneration occurs very slowly, and it can take years for symptoms to appear.…”

Unlocking the Potential: Semaglutide’s Impact on Alzheimer’s and Parkinson’s Disease in Animal Models

“…The pathological disturbances in AD are multifaceted and involve a combination of genetic, molecular, and cellular mechanisms. The primary pathological hallmarks of AD include amyloid-beta (Aβ) plaques, neurofibrillary tangles (NFTs), neuroinflammation, and synaptic and neuronal loss [ 69 ].…”

Association of CHAT Gene Polymorphism rs3793790 and rs2177370 with Donepezil Response and the Risk of Alzheimer’s Disease Continuum

“… 1 Characteristic pathological changes have occurred in the brain before the patient has clinical symptoms, and amyloid β-protein (Aβ) deposition and hyperphosphorylated tau protein are key links of AD pathogenesis. 2 As pathological changes such as Aβ and tau continue to worsen, the appearance and progression of clinical symptoms are eventually elicited. 3 Therefore, it is considered to be an Alzheimer’s disease continuum (ADC) rather than an entity.…”