scholarly journals Treatment of Alzheimer’s Disease: Current Management and Experimental Therapeutics

2013 ◽  
Vol 2 (3) ◽  
pp. 174-181 ◽  
Author(s):  
Lawrence S. Honig ◽  
Clara D. Boyd
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Experimental Therapeutics ◽  
Current Management

scholarly journals Enhancing α-secretase Processing for Alzheimer’s Disease—A View on SFRP1

2020 ◽  
Vol 10 (2) ◽  
pp. 122 ◽  
Author(s):  
Bor Luen Tang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Experimental Therapeutics ◽  
Related Protein ◽  
Endogenous Inhibitor ◽  
Aβ Peptides ◽  
App Processing ◽  
Promising Therapeutic Target ◽  
A Disintegrin And Metalloproteinase

Amyloid β (Aβ) peptides generated via sequential β- and γ-secretase processing of the amyloid precursor protein (APP) are major etiopathological agents of Alzheimer’s disease (AD). However, an initial APP cleavage by an α-secretase, such as the a disintegrin and metalloproteinase domain-containing protein ADAM10, precludes β-secretase cleavage and leads to APP processing that does not produce Aβ. The latter appears to underlie the disease symptom-attenuating effects of a multitude of experimental therapeutics in AD animal models. Recent work has indicated that an endogenous inhibitor of ADAM10, secreted-frizzled-related protein 1 (SFRP1), is elevated in human AD brains and associated with amyloid plaques in mouse AD models. Importantly, genetic or functional attenuation of SFRP1 lowered Aβ accumulation and improved AD-related histopathological and neurological traits. Given SFRP1′s well-known activity in attenuating Wnt signaling, which is also commonly impaired in AD, SFRP1 appears to be a promising therapeutic target for AD. This idea, however, needs to be addressed with care because of cancer enhancement potentials resulting from a systemic loss of SFRP1 activity, as well as an upregulation of ADAM10 activity. In this focused review, I shall discuss α-secretase-effected APP processing in AD with a focus on SFRP1, and explore the contrasting perspectives arising from the recent findings.

Role of Alzheimer's disease models in designing and testing experimental therapeutics

2005 ◽  
Vol 2 (4) ◽  
pp. 305-312 ◽  
Author(s):  
Alena V. Savonenko ◽  
Fiona M. Laird ◽  
Juan C. Troncoso ◽  
Philip C. Wong ◽  
Donald L. Price
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Models ◽  
Experimental Therapeutics

scholarly journals A Review on Potential Mechanisms ofTerminalia chebulain Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Amir R. Afshari ◽  
Hamid R. Sadeghnia ◽  
Hamid Mollazadeh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Medicinal Plant ◽  
Wide Spectrum ◽  
Acetylcholinesterase Inhibitors ◽  
Current Management ◽  
Chebulagic Acid ◽  
Herbal Plants ◽  
Medicinal Properties ◽  
Therapeutic Alternatives

The current management of Alzheimer’s disease (AD) focuses on acetylcholinesterase inhibitors (AChEIs) and NMDA receptor antagonists, although outcomes are not completely favorable. Hence, novel agents found in herbal plants are gaining attention as possible therapeutic alternatives. TheTerminalia chebula(Family: Combretaceae) is a medicinal plant with a wide spectrum of medicinal properties and is reported to contain various biochemicals such as hydrolysable tannins, phenolic compounds, and flavonoids, so it may prove to be a good therapeutic alternative. In this research, we reviewed published scientific literature found in various databases: PubMed, Science Direct, Scopus, Web of Science, Scirus, and Google Scholar, with the keywords:T. chebula, AD, neuroprotection, medicinal plant, antioxidant, ellagitannin, gallotannin, gallic acid, chebulagic acid, and chebulinic acid. This review shows thatT. chebulaextracts and its constituents have AChEI and antioxidant and anti-inflammatory effects, all of which are currently relevant to the treatment of Alzheimer’s disease.

Alzheimer’s Disease

2017 ◽  
Author(s):  
Gregory A. Jicha ◽  
Frederick A. Schmitt
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Biology ◽  
Focal Point ◽  
Treatment Strategies ◽  
Limited Evidence ◽  
Current Management ◽  
Symptomatic Management ◽  
Clinical Benefits ◽  
Experimental Disease

Advances in the current management and treatment of Alzheimer’s disease have grown directly from our increased understanding of the neurobiology underlying this disease. Currently available pharmacologic and nonpharmacologic treatment strategies remain focused on symptomatic management of disease rather than disease modification. Despite a wealth of evidence supporting the clinical benefits of existing therapies in the management of symptomatic progression, there is limited evidence that these available therapies modify disease progression over the course of dementia progression. More recent research discoveries in the areas of genetics, molecular and cell biology, and environmental risk factors have become the focal point for an explosive growth in experimental disease-modifying strategies designed to prevent, slow, or potentially halt the progression of Alzheimer’s disease.

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