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Through tyrosine phosphorylation, subcellular translocation, regulation of its expression, and caspase-3-dependent proteolytic activation, PKC\u03b4 can convert transient adaptive responses into sustained oxidative, mitochondrial, inflammatory, and nuclear apoptotic signaling. This review evaluates PKC\u03b4 across Parkinson\u2019s disease (PD), Alzheimer\u2019s disease (AD), Huntington\u2019s disease (HD), and ischemic stroke, emphasizing disease- and cell type-specific mechanisms rather than a uniformly pathogenic role. In PD, PKC\u03b4 most consistently amplifies toxin- and \u03b1-synuclein-associated dopaminergic injury and glial inflammation, although human evidence remains limited. In AD, PKC\u03b4 may link amyloidogenic processing of amyloid precursor protein (APP), amyloid-beta peptide (A\u03b2)-induced neuronal stress\/cell cycle reentry, and glial neuroinflammation in a context-dependent feed-forward circuit. In HD, PKC\u03b4 signaling may shift from early compensatory downregulation to stress-induced apoptotic reactivation. In ischemic stroke, the strongest evidence implicates PKC\u03b4 in reperfusion-associated oxidative and inflammatory injury, particularly through neutrophil and translocation-dependent mechanisms. Future therapeutic development will require isoform-selective, compartment-specific, and cell type-resolved PKC\u03b4 modulation.<\/jats:p>","DOI":"10.1007\/s12013-026-02125-w","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T13:06:59Z","timestamp":1787576819000},"page":"3245-3271","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Protein Kinase C-delta (PKC\u03b4) in Neurodegeneration and Cerebral Ischemia: Molecular Mechanisms and Therapeutic Implications"],"prefix":"10.1007","volume":"84","author":[{"given":"Yi-Heng","family":"Hsieh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I-Yen","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"You","family":"Lien","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lon-Fye","family":"Lye","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yen-Chuan","family":"Ou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5544-7561","authenticated-orcid":false,"given":"Ding-I","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,24]]},"reference":[{"key":"2125_CR1","doi-asserted-by":"publisher","first-page":"105692","DOI":"10.1016\/j.jbc.2024.105692","volume":"300","author":"MG Kazanietz","year":"2024","unstructured":"Kazanietz, M. 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