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This review synthesizes compelling evidence that positions astrocyte dysfunction, or astrocytopathy, as a central and active driver of pathogenesis, extending far beyond a passive bystander role. We delineate how pathological \u03b1-synuclein triggers a vicious cycle of astrocytic failure, encompassing impaired proteostasis via ubiquitin-proteasome and autophagy-lysosomal pathways, glymphatic system collapse due to aquaporin-4 (AQP4) depolarization, and chronic neuroinflammation driven by microglial crosstalk and NLRP3 inflammasome activation. This core triad is exacerbated by critical deficits in metabolic support, including disruption of the astrocyte-neuron lactate shuttle, aberrant lipid droplet metabolism, and failure in mitochondrial transfer. Furthermore, we integrate emerging systemic axes, demonstrating how peripheral gut dysbiosis, via the microbiota-gut-astrocyte (MGA) axis, and central circadian rhythm disruption converge to amplify central glial pathology. Critically, the present reframing unveils novel, cell-type-specific therapeutic avenues. We evaluate strategies to restore neuroprotection by targeting AQP4 polarization, modulating GLP-1 receptor signaling to mitigate inflammation, employing senolytics to clear dysfunctional glia, and utilizing gene therapy to engineer astrocytes as trophic bio-factories. By deconstructing PD as a disorder of astrocyte-neuron crosstalk, this review provides a roadmap for next-generation, disease-modifying therapies aimed at rescuing glial homeostasis to halt progression, moving beyond symptomatic dopamine replacement to address the core pathophysiology.<\/jats:p>","DOI":"10.1007\/s12035-026-06177-0","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T02:53:38Z","timestamp":1790045618000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Convergent Astrocytic Failure in Parkinson\u2019s Disease: A System-Level Model of Pathogenesis and Treatment"],"prefix":"10.1007","volume":"63","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4747-8549","authenticated-orcid":false,"given":"Ahmed M.","family":"Abdelaziz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed N.","family":"Fawzy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mustafa M.","family":"Shokr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,22]]},"reference":[{"key":"6177_CR1","doi-asserted-by":"publisher","unstructured":"El-Sayed RM, Abdelaziz  AM, Zaki  HF, Abdel Rasheed\u00a0NO (2023) Cilostazol novel neuroprotective mechanism against rotenone-induced Parkinson\u2019s disease in rats: correlation between Nrf2 and HMGB1\/TLR4\/PI3K\/Akt\/mTOR signaling. 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