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Born to Protect: Leveraging BDNF Against Cognitive Deficit in Alzheimer's Disease.
CNS Drugs ( IF 7.4 ) Pub Date : 2020-03-01 , DOI: 10.1007/s40263-020-00705-9
Lucia Caffino 1 , Francesca Mottarlini 1 , Fabio Fumagalli 1
Affiliation  

Alzheimer's disease is a chronic neurodegenerative devastating disorder affecting a high percentage of the population over 65 years of age and causing a relevant emotional, social, and economic burden. Clinically, it is characterized by a prominent cognitive deficit associated with language and behavioral impairments. The molecular pathogenesis of Alzheimer's disease is multifaceted and involves changes in neurotransmitter levels together with alterations of inflammatory, oxidative, hormonal, and synaptic pathways, which may represent a drug target for both prevention and treatment; however, an effective treatment for Alzheimer's disease still represents an unmet goal. As neurotrophic factors participate in the modulation of the above-mentioned pathways, they have been highlighted as critical contributors of Alzheimer's disease etiology, whose modulation might be beneficial for Alzheimer's disease. We focused on the neurotrophin brain-derived neurotrophic factor, providing several lines of evidence pointing to brain-derived neurotrophic factor as a plausible endophenotype of cognitive deficits in Alzheimer's disease, illustrating some of the most recent possibilities to modulate the expression of this neurotrophin in the brain in an attempt to ameliorate cognition and delay the progression of Alzheimer's disease. This review shows that otherwise disparate pharmacologic or non-pharmacologic approaches converge on brain-derived neurotrophic factor, providing a means whereby apparently unrelated medical approaches may nevertheless produce similar synaptic and cognitive outcomes in Alzheimer's disease pathogenesis, suggesting that brain-derived neurotrophic factor-based synaptic repair may represent a modifying strategy to ameliorate cognition in Alzheimer's disease.

中文翻译:

为保护自己而生:利用BDNF对抗阿尔茨海默氏病的认知缺陷。

阿尔茨海默氏病是一种慢性神经退行性破坏性疾病,在65岁以上的人群中占很大比例,并造成相关的情感,社会和经济负担。在临床上,它的特征是与语言和行为障碍相关的明显认知缺陷。阿尔茨海默氏病的分子发病机制是多方面的,涉及神经递质水平的变化以及炎症,氧化,激素和突触途径的改变,这可能代表了预防和治疗的药物靶点;然而,有效的阿尔茨海默氏病治疗方法仍未达到目标。由于神经营养因子参与上述途径的调节,因此它们被认为是阿尔茨海默氏病的关键因素。病的病因,其调节可能对阿尔茨海默氏病有益。我们专注于神经营养因子脑源性神经营养因子,提供了多条证据表明脑源性神经营养因子是阿尔茨海默氏病认知缺陷的合理内表型,说明了调节该神经营养蛋白在脑组织中表达的最新可能性。试图改善认知并延缓阿尔茨海默氏病的发展。这项审查表明,其他形式上不同的药物或非药物方法都集中在脑源性神经营养因子上,提供了一种手段,尽管如此,显然无关的医学方法仍可能在阿尔茨海默氏病的发病机理中产生相似的突触和认知结果,
更新日期:2020-02-12
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