Review for "Novel therapeutic strategies for Alzheimer’s disease targeting brain cholesterol homeostasis"

Author(s):  
jacques Fantini
2003 ◽  
Vol 24 (5) ◽  
pp. 233-238 ◽  
Author(s):  
Andrea Caricasole ◽  
Agata Copani ◽  
Alessandra Caruso ◽  
Filippo Caraci ◽  
Luisa Iacovelli ◽  
...  

Author(s):  
Angeles Tecalco–Cruz ◽  
Jesús Zepeda–Cervantes ◽  
Lilia López-Canovas ◽  
Josué O. Ramírez–Jarquín ◽  
José Pedraza-Chaverrí ◽  
...  

: Alzheimer's disease (AD) is characterized by progressive memory loss due to neurodegeneration that occurs mainly during aging. The accumulation of senescent cells has been related to aging. Furthermore, the expression of the variant ApoE ∈ 4 is a critical risk factor for AD. Some events that occur in senescence, such as the secretion of pro-inflammatory molecules, and metabolic and epigenetic changes, in addition to the detection of ApoE4, may accelerate the progression of AD. Here, we discuss the implications of cellular senescence and the presence of ApoE polymorphisms in AD. Molecular studies of these risk factors for AD may hence be pivotal to define new biomarkers and novel therapeutic strategies for this neurodegenerative pathology.


Author(s):  
S. Imindu Liyanage ◽  
Prachi Vilekar ◽  
Donald F. Weaver

AbstractIn recent decades, clinical trials in Alzheimer’s disease (AD) have failed at an unprecedented rate. The etiology of AD has since come under renewed scrutiny, both to elucidate the underlying pathologies and to identify novel therapeutic strategies. Here, diet has emerged as a potential causative/protective agent. A variety of nutrients, including lipids, minerals, vitamins, antioxidants and sugars as well as broader dietary patterns and microbiotal interactions have demonstrated associations with AD. Although clinical trials have yet to definitively implicate any singular dietary element as therapeutic or causative, it is apparent that dietary preferences, likely in complex synergies, may influence the risk, onset and course of AD. This review catalogs the impact of major dietary elements on AD. It further examines an unexplored reciprocal association where AD may modulate diet, as well as how potential therapeutics may complicate these interactions. In doing so, we observe diet may have profound effects on the outcome of a clinical trial, either as a confounder of a drug/disease interaction or as a generally disruptive covariate. We therefore conclude that future clinical trials in AD should endeavor to control for diet, either in study design or subsequent analyses.


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