Mechanistic convergence of Astragalus-derived phytochemicals in Alzheimer's disease: A systematic review.

Alzheimer’s Disease (AD) represents a systems-level failure of interacting neurobiological pathways rather than a single-target pathology. Its neuropathology is defined by extracellular β-amyloid (Aβ) plaques, intracellular neurofibrillary tangles (formed by hyperphosphorylated tau proteins), and widespread neuroinflammation (). Despite decades of efforts, the currently approved therapeutics such as donepezil, rivastigmine, and memantine only provide symptomatic relief without reversing or even halting neurodegeneration. The complexity of AD pathogenesis, involving an array of neurophysiological disturbances including but not limited to oxidative stress (), mitochondrial dysfunction, and iron dyshomeostasis and subsequent ferroptosis () highlights the need for multi-target therapeutic strategies. Because the included studies investigated extracts and phytochemicals derived from multiple , this review uses the general term except where a study specifies a particular species. has traditionally been prescribed for fatigue, immune weakness, and age-associated cognitive decline, and is frequently incorporated into multi-herb formulations aimed at restoring ‘Qi’ and systemic vitality. From a pharmacological perspective, this traditional rationale aligns with emerging evidence that complex phytochemical mixtures may exert network-level modulation of neuroinflammatory and oxidative stress pathways. Such multi-target activity is particularly relevant in AD, where oxidative stress, mitochondrial dysfunction, neuroimmune activation, and amyloidogenic processing interact in a self-reinforcing pathological cascade.