دورية أكاديمية
أعرض في EDS

Novel Leptin-Based Therapeutic Strategies to Limit Synaptic Dysfunction in Alzheimer's Disease.

التفاصيل البيبلوغرافية
العنوان: Novel Leptin-Based Therapeutic Strategies to Limit Synaptic Dysfunction in Alzheimer's Disease.
المؤلفون: Harvey J; Department of Neuroscience, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2024 Jul 04; Vol. 25 (13). Date of Electronic Publication: 2024 Jul 04.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Alzheimer Disease*/metabolism , Alzheimer Disease*/drug therapy , Leptin*/metabolism , Synapses*/metabolism, Humans ; Animals ; Amyloid beta-Peptides/metabolism ; tau Proteins/metabolism ; Receptors, Leptin/metabolism ; Hippocampus/metabolism
مستخلص: Accumulation of hyper-phosphorylated tau and amyloid beta (Aβ) are key pathological hallmarks of Alzheimer's disease (AD). Increasing evidence indicates that in the early pre-clinical stages of AD, phosphorylation and build-up of tau drives impairments in hippocampal excitatory synaptic function, which ultimately leads to cognitive deficits. Consequently, limiting tau-related synaptic abnormalities may have beneficial effects in AD. There is now significant evidence that the hippocampus is an important brain target for the endocrine hormone leptin and that leptin has pro-cognitive properties, as activation of synaptic leptin receptors markedly influences higher cognitive processes including learning and memory. Clinical studies have identified a link between the circulating leptin levels and the risk of AD, such that AD risk is elevated when leptin levels fall outwith the physiological range. This has fuelled interest in targeting the leptin system therapeutically. Accumulating evidence supports this possibility, as numerous studies have shown that leptin has protective effects in a variety of models of AD. Recent findings have demonstrated that leptin has beneficial effects in the preclinical stages of AD, as leptin prevents the early synaptic impairments driven by tau protein and amyloid β. Here we review recent findings that implicate the leptin system as a potential novel therapeutic target in AD.
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معلومات مُعتمدة: AS-PhD-18-007 United Kingdom ALZS_ Alzheimer's Society
فهرسة مساهمة: Keywords: AMPA; hippocampus; leptin; receptor trafficking; synaptic plasticity; tau
المشرفين على المادة: 0 (Leptin)
0 (Amyloid beta-Peptides)
0 (tau Proteins)
0 (Receptors, Leptin)
تواريخ الأحداث: Date Created: 20240713 Date Completed: 20240713 Latest Revision: 20240715
رمز التحديث: 20240715
مُعرف محوري في PubMed: PMC11242278
DOI: 10.3390/ijms25137352
PMID: 39000459
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms25137352