Alzheimer's Disease: From Animal Models to the Human Syndrome

Abstract

Some animal models, genetically modified (such as murine) and sporadic (as others species), enable the study of the origin of specific lesions observed in human neurodegenerative diseases. In particular, Alzheimer's disease (AD) models have been designed to test the hypothesis that certain lesions are associated with functional and morphological changes beginning with memory loss and impairment in activities of daily life. This review compares and evaluates the phenotypes of different AD animal models, on the basis of the specific objectives of each study, with the purpose of encompassing their contributions to the comprehension of the AD signs and symptoms in humans. All these models contribute to the comprehension of the human AD mechanisms regarding the heterogeneity of AD phenotypes: the overlap between AD and age-related changes, the variability of AD onset (early or late), the probable reactiveness of amyloid-β and tau proteins, the scarcity of senile plaques and/or neurofibrillary tangles in some AD cases, the spatial correlation of the pathology and cerebral blood vessels, and the immunological responses (microglial aging) and synaptopathy. Altogether, these considerations may contribute to find therapies to treat and prevent this disease.

Reactions of a Polyhalide Ionic Liquid with Copper, Silver, and Gold

“…[5] Moreover,t hey also exhibit stereo- [6] and regioselectivity, [7] and the reusability of some of these agentsh as been demonstrated. [6][7][8] In addition, IL-based polyhalides have great potential as "green" halogenation reagents due to their low volatility, which makes them easier to handle than the base halogens. Another application for trihalide ionicl iquids is relatedt ot he electrolyte in dye-sensitized solarc ells (DSSCs).…”

Studies for Improving a Rat Model of Alzheimer’s Disease: Icv Administration of Well-Characterized β-Amyloid 1-42 Oligomers Induce Dysfunction in Spatial Memory

“…A great variety of first- and second-generation transgenic mouse models of AD have been developed during the last 20 years for studying the pathophysiological processes of the disease, as reviewed in [ 25 , 26 , 27 , 28 , 29 , 30 , 31 ]. The transgenic mouse and knockout models analyze certain aspects of AD pathology, allowing exploration of unknown territories and revealing new pathogenic possibilities [ 32 ]. Summaries of the most prominent mouse models of AD have been published very recently [ 31 , 33 , 34 ].…”

Alzheimer's disease‐like neuropathology in three species of oceanic dolphin

“…Studies in the brains of human patients remain the most critical route for characterizing and understanding the condition as AD appears to be exclusive to humans (Walker & Jucker, 2017; Youssef et al, 2016), and the absence of an accurate, valid experimental animal model, spontaneous or induced and that completely captures the human phenotype, has hindered research on the etiology and pathogenesis of the disease. Furthermore, studies using these incomplete (including transgenic) animal models have yielded contradicting results thereby impeding progress in developing potential treatments (Orta‐Salazar et al, 2016).…”