{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T01:47:01Z","timestamp":1793843221028,"version":"4.6.1"},"reference-count":138,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T00:00:00Z","timestamp":1761609600000},"content-version":"vor","delay-in-days":27,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid\u2010beta (A\u03b2) deposition and tau pathology. Although disease\u2010modifying therapies, such as anti\u2010A\u03b2 monoclonal antibodies, have been approved, their clinical efficacy remains modest and accompanied by substantial safety concerns. The glymphatic system, which is a brain\u2010wide waste clearance network mediated by cerebrospinal fluid\u2010interstitial fluid exchange, is critical in AD pathogenesis. Glymphatic dysfunction promotes A\u03b2 and tau accumulation, neuroinflammation, and vascular impairment, forming a vicious cycle that drives neurodegeneration. This review elucidates the anatomical and physiological basis of the glymphatic system, its role in AD progression, and novel therapeutic strategies targeting glymphatic enhancement. Emerging interventions, including aquaporin\u20104 (AQP4) modulation, meningeal lymphatic regeneration, cervical deep lymphaticovenous anastomosis, and nonpharmacological approaches, are also discussed for their potential to shift AD therapeutics from symptom management to disease modification.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Glymphatic dysfunction drives Alzheimer's disease (AD) pathogenesis.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Meningeal lymphatic decline with aging.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Cervical lymphaticovenous anastomosis (LVA) as novel new intervention method for patients with AD<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The apolipoprotein E (APOE) \u03b54 allele disrupts meningeal lymphatic function, increasing AD risk via amyloid\u2010\u03b2 (A\u03b2) clearance deficits.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Diffusion tensor imaging along the perivascular space (DTI\u2010ALPS) and dynamic magnetic resonance imaging (MRI) enable early detection of glymphatic dysfunction, guiding pre\u2010symptomatic AD interventions.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Sleep and arterial pulsatility critically regulate glymphatic efficiency, offering non\u2010pharmacological therapeutic avenues.<\/jats:p>\n                        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