Biotechnological Perspectives on GSK-3β and Hyperprolactinemia: Implications for the Progression of Alzheimer’s Disease

Background:: Alzheimer's Disease (AD) is a progressive neurodegenerative condition, which is typified by the extracellular presence of amyloid-B (A2) in the form of plaques, intracellular neurofibrillary tangles, which are made up of hyperphosphorylated tau, and deterioration of mental abilities. Glycogen synthase kinase-3 beta (GSK-3β) is also one of the molecular drivers that have been implicated in AD pathogenesis due to its contributions to tau hyperphosphorylation, Aβ production, and synaptic dysfunction. There is accumulating evidence suggesting that endocrine dysregulation and hyperprolactinemia, characterized by elevated circulating prolactin levels, may contribute to neurodegeneration through dopaminergic imbalance, oxidative stress, and neuroinflammation. Methods:: Recent peer-reviewed literature on the mechanistic intersections of GSK-32 signaling, hyperprolactinemia, and AD pathology was reviewed through a narrative synthesis. The research assessing hormonal regulation of neuroinflammatory cascades, dopaminergic tone, and structural changes in the brain was reviewed to identify potentially realistic biological relationships. Results:: It was found that inhibitory control of GSK-3b could be reduced by hyperprolactinemiainduced dopamine depletion, leading to increased GSK-3 b activity. This deregulation may increase tau phosphorylation and inflammatory reactions, which develop AD disease. Also, prolactinmediated oxidative stress may impair neuronal integrity. Discussion:: Hormonal imbalance and dysregulation of kinases are attractive therapeutic targets. Dopamine agonists can potentially reestablish dopaminergic suppression of GSK-3 2, whereas GSK-3 2 inhibitors have the potential to directly suppress tau pathology. A dual-modality approach can be beneficial in synergy, as it considers not only the neuroendocrine dimensions of AD but also the neurodegenerative. Conclusion:: Hyperprolactinemia may be an under-researched factor in the pathogenesis of AD. This clarification would guide the development of biomarkers and new, stratified interventions capable of going beyond traditional amyloid- and tau-based interventions.