Utility of Animal Models to Understand Human Alzheimer’s Disease, Using the Mastermind Research Approach to Avoid Unnecessary Further Sacrifices of Animals.
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Utility of Animal Models to Understand Human Alzheimer’s Disease, Using the Mastermind Research Approach to Avoid Unnecessary Further Sacrifices of Animals.
To diagnose and treat early stages (preclinical) Alzheimer’s disease (AD) patients, we need the body-fluid-based biomarkers that reflect the processes that occur at this stage, but the current knowledge on the processes associated less. As human studies on the (possible) onset and early stage AD would be very expensive and time consuming, we investigated the potential value of animal models of AD to help fill this knowledge gap.
We provide a comprehensive overview of the processes associated with AD pathogenesis and biomarkers, the current knowledge on biomarker-associated AD comes from the brains of humans and animals and body fluids, comparison of biomarkers obtained in AD human and frequently used animal model of AD, and appeared body-fluid-based biomarkers. In human studies, amyloid beta (Aβ), hyperphosphorylated tau (P-tau), the amount of tau (T-tau), neurogranin, SNAP-25, glial fibrillary acidic protein (GFAP), YKL-40, and especially light Neurofilament (NFL ) is often measured. In animal studies, the emphasis was largely on Aβ.
Although a direct comparison between human AD (familial and sporadic) and (largely genetic) animal models of AD can not be made, still, in the brain, cerebrospinal fluid (CSF), and blood, the majority of similar trends were observed for stage AD humans and AD animal stage Model life. This shows the potential value of animal models in understanding the early stages of AD and the beginning of AD. In addition, animal studies can be intelligently designed to provide mechanistic information about the interrelationships between the different processes longitudinally AD and may also include a combination of the different conditions which may reflect comorbidity in human AD, according to Research Mastermind approach.
It may not be surprising that the brain as an organ rich in lipids show impaired lipid profile in neurodegenerative conditions such as Alzheimer’s disease. It is, however, more challenging to detect these changes because they may only occur in a small spatial area. Editorial highlights work by Rich et al. using a technology called MALDI IMS raising to identify the up or downregulation of specific lipids in and around the amyloid plaques, one of the pathological hallmarks of Alzheimer’s disease.
Interestingly, lipid changes as it parallel to the structure of myelin interrupted just at the border between white matter and gray.
Utility of Animal Models to Understand Human Alzheimer’s Disease, Using the Mastermind Research Approach to Avoid Unnecessary Further Sacrifices of Animals.
Multifunction Glycogen Synthase Kinase Ligands with Inhibitory Activity 3 as a New Direction in Alzheimer’s Disease Drug Research.
Alzheimer’s disease (AD) belong to the most common form of dementia that causes progressive loss of brain cells and leads to memory impairment and decreased ability to think more. There has been no effective treatment for AD; Therefore, the search for new drugs that can improve memory and other cognitive functions is one of the hot research topic worldwide. Scientific efforts are also directed combat the behavioral and psychological symptoms of dementia, which is an integral part of the disease.
Several studies have shown that glycogen synthase kinase 3 beta (GSK3β) plays an important role in the pathogenesis of AD. In addition, inhibition of GSK3β provided beneficial effects on memory enhancement in several animal models of AD. This review aims to update the most recent report on the discovery of novel multifunctional ligands with GSK3β inhibitory activity as potential drugs for the treatment of symptoms and disease-modifying AD.
Description: Human amygdala tissue lysate was prepared by homogenization using a proprietary technique. The tissue was frozen in liquid nitrogen immediately after excision and then stored at -70°C. The human amygdala tissue total protein is provided in a buffer including HEPES (pH7.9), MgCl2, KCl, EDTA, Sucrose, Glycerol, Sodium deoxycholate, NP-40, and a cocktail of protease inhibitors. For quality control purposes, the amygdala tissue pattern on SDS-PAGE gel is shown to be consistent for each lot by visualization with coomassie blue staining. The amygdala tissue is then Western analyzed by either GAPDH or β-actin antibody, and the expression level is consistent with each lot.
Description: Human brain amygdala tissue membrane protein lysate was prepared by isolating the membrane protein from whole tissue homogenates using a proprietary technique. The human amygdala tissue was frozen in liquid nitrogen immediately after excision and then stored at -70°C. The membrane protein is provided in a buffer including HEPES (pH 7.9), MgCl2, KCl, EDTA, Sucrose, Glycerol, sodium deoxycholate, NP-40, and a cocktail of protease inhibitors. For quality control purposes, the isolated brain amygdala tissue membrane protein pattern on SDS-PAGE gel is shown to be consistent for each lot by visualization with coomassie blue staining. The isolated brain amygdala tissue membrane protein is then Western analyzed by either GAPDH or β-actin antibody to confirm there is no signal or very weak signal.
GSK3β inhibitory activity of compounds with pharmacological approach appears to be effective for treating the causes and symptoms of AD because they reduce neuroinflammation and pathological excellence in animal models of AD and provide relief from cognitive and neuropsychiatric symptoms. These compounds have the potential to be used as a drug for the treatment of AD, but their exact pharmacological, pharmacokinetic, toxicology and clinical profile needs to be defined.
