Therapeutic Strategies Aimed at Improving Neuroplasticity in Alzheimer Disease

被引:6
|
作者
Colavitta, Maria F. [1 ,2 ]
Barrantes, Francisco J. [1 ]
机构
[1] Univ Catolica Argentina UCA, Biomed Res Inst BIOMED, Natl Sci & Tech Res Council CONICET, Lab Mol Neurobiol, C1107AAZ, Buenos Aires, Argentina
[2] Ctr Invest Psicol & Psicopedag CIPP UCA, Fac Psicol, Ave Alicia Moreau de Justo,C1107AAZ, Buenos Aires, Argentina
关键词
Alzheimer disease; cognition; neuroplasticity; neurotransmitters; long-term potentiation; cognitive impairment: animal models; dementias; neurodegenerative diseases; neuroinflammation; therapeutics; NICOTINIC ACETYLCHOLINE-RECEPTORS; LONG-TERM POTENTIATION; AMYLOID-BETA-PROTEIN; MILD COGNITIVE IMPAIRMENT; SYNAPTIC PLASTICITY; A-BETA; TRANSGENIC MODEL; ALLOSTERIC POTENTIATION; CHOLINERGIC HYPOTHESIS; SOLUBLE OLIGOMERS;
D O I
10.3390/pharmaceutics15082052
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Alzheimer disease (AD) is the most prevalent form of dementia among elderly people. Owing to its varied and multicausal etiopathology, intervention strategies have been highly diverse. Despite ongoing advances in the field, efficient therapies to mitigate AD symptoms or delay their progression are still of limited scope. Neuroplasticity, in broad terms the ability of the brain to modify its structure in response to external stimulation or damage, has received growing attention as a possible therapeutic target, since the disruption of plastic mechanisms in the brain appear to correlate with various forms of cognitive impairment present in AD patients. Several pre-clinical and clinical studies have attempted to enhance neuroplasticity via different mechanisms, for example, regulating glucose or lipid metabolism, targeting the activity of neurotransmitter systems, or addressing neuroinflammation. In this review, we first describe several structural and functional aspects of neuroplasticity. We then focus on the current status of pharmacological approaches to AD stemming from clinical trials targeting neuroplastic mechanisms in AD patients. This is followed by an analysis of analogous pharmacological interventions in animal models, according to their mechanisms of action.
引用
收藏
页数:23
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