Alzheimer's disease-associated genes expression: A new direction in the ischemic etiology and therapy of Alzheimer's disease

Increasing evidence supports a link between brain ischemia and the development of Alzheimer’s disease (AD). Experimental and clinical studies have shown that ischemic episodes trigger the overexpression of genes associated with AD pathology, including amyloid precursor protein (APP), β-secretase (BACE1), presenilin 1 and 2, and tau protein. These changes promote beta-amyloid peptide accumulation, neurofibrillary tangle formation, and progressive neurodegeneration in patterns that closely mirror the hallmarks of AD. Despite growing recognition that ischemia-reperfusion injury may represent a critical upstream trigger for AD-type pathology, the molecular cascades linking ischemic gene dysregulation to sustained neurodegeneration remain incompletely understood. This gap limits the development of targeted therapies that could intervene at the vascular and ischemic level to slow or prevent the onset of AD.This Research Topic aims to consolidate current knowledge and stimulate new research on the role of AD-associated gene expression changes following brain ischemia, and to explore how these insights can inform novel therapeutic strategies. By bringing together studies on post-ischemic alterations in APP, tau protein, secretases, and presenilins gene expression, this collection will map the molecular landscape that connects cerebral ischemia to AD-type neurodegeneration. A central objective is to evaluate whether ischemia-induced genes dysregulation represents a modifiable therapeutic target, opening avenues for pharmacological, genetic, or neuroprotective interventions. This Research Topic also seeks to bridge the gap between experimental ischemia models and clinical observations in patients with cerebrovascular diseases who develop dementia, with the goal of fostering translational approaches that address the vascular contribution to AD etiology.To gather further insights into the ischemic mechanisms driving AD-associated genes expression and their therapeutic implications, we welcome articles addressing, but not limited to, the following themes:• Post-ischemic expression of APP, tau protein, presenilins, and secretases genes in experimental and clinical settings• Molecular pathways linking ischemia-reperfusion injury to beta-amyloid peptide generation and tau protein hyperphosphorylation• Neuroinflammatory and oxidative stress responses as mediators of ischemia-induced AD genes dysregulation• Neuroprotective and pharmacological strategies targeting ischemia-driven AD neuropathology• Biomarkers of post-ischemic neurodegeneration with relevance to early AD detection• Epidemiological and clinical evidence connecting cerebrovascular disease, brain ischemia, and AD progression• Comparative analysis of genes expression profiles in ischemic brain injury versus sporadic ADWe encourage a wide range of submissions, including original research, methods papers, brief research reports, data reports, systematic reviews, mini reviews and perspectives. Topic editors: Ryszard Pluta, Marzena Ułamek-Kozioł Source: https://www.frontiersin.org/research-topics/80298/alzheimers-disease-associated-genes-expression-a-new-direction-in-the-ischemic-etiology-and-therapy-of-alzheimers-disease