Alzheimer disease animal model

Key Words 5-HT6 receptors Alzheimer disease animal models cognition schizophrenia. 

Treatment of Alzheimer s disease animal models with metal ligands. 125... 

Frydman-Marom, A., Levin, A., Farfara, D., Benromano, T., Scherzer-Attali, R., Peled, S., and Ovadia, M. 2011. Orally administrated cinnamon extract reduces p-amyloid oligomerization and corrects cognitive impairment in Alzheimer s disease animal models. PloS One, 6(1), el6564. 

According to the amyloid hypothesis, the A 3 peptide plays a critical role in the pathogenesis of Alzheimer s disease [1]. Major forms of A 3 produced encompass 38, 40 or 42 residues. A 342 is more prone to aggregation than A 340 and in animal models an increased A[342/ A (340 ratio results in amyloid plaque pathology even when total A 3 levels are reduced [4]. The generation of A 3 is a normal process and A 3 is present in the brains and body fluids of humans throughout life. Neuronal... 

Alzheimer s disease (AD) 2. In the hippocampus of p-amylo id-treated rats, an animal model of AD, 2-AG levels are elevated and exert neuroprotection but also participate in memory retention loss 2. Inhibitors of cellular re-uptake or CB-, antagonists, possibly depending on the phase of the disorder... 

Curcumin (diferuloyl methane) is the main pigment of turmeric. It is widely used as a colorant and preservative agent. No data regarding its daily intake in western countries are available intake may reach 80 to 200 mg in adult Indians. To date, no study has explored the effect of curcumin consumption on the incidence of diseases, but many beneficial effects on health have been reported in cell and animal models. These include anti-carcinogenic, anti-diabetic, anti-atherosclerotic, and anti-Alzheimer s disease properties. ... 

McDonald MP and Overmier JB (1998). Present imperfect A critical review of animal models of the mnemonic impairments in Alzheimer s disease. Neuroscience and Biobehavioral Reviews, 22, 99-120. 

Morgan, D., Diamond, D. M., Gottschall, P. E. et al. A(3 peptide vaccination prevents memory loss in an animal model of Alzheimer s disease. Nature 408 982-985, 2000. 

Since the early 1980s, much effort has focused on animal models of acute and chronic neurodegeneration in search of therapeutics for stroke. Neuronal cell death follows strokes, acute ischemic insults, and chronic neurodegeneration, such as Parkinson s disease, Alzheimer s disease (AD), epilepsy, and Huntington s disease. Up to 80% of all strokes result from focal infarcts and ischemia in the middle cerebral artery (MCA), so the commonly used animal models for neuroprotection are produced by temporary or permanent occlusion of the MCA.5 Lesions of the MCA include occlusion by electrocoagulation, intraluminal monofilaments, photochemical effects, thrombosis, and endothelin-1, but all of these models necessitate studying reperfusion events and validating MCA occlusion by behavioral assessments. 

Tuszynski, M.H. and Blesch, A., Nerve growth factor from animal models of cholinergic neuronal degeneration to gene therapy in Alzheimer s disease, Prog. Brain. Res., 146, 441, 2004. 

Little is formally known about the toxicity of amanita use. Ibotenic acid is a potent neurotoxin, through excitatory amino acid mechanisms (Steiner et al. 1984 Schwarcz et al. 1984). It has been used extensively in animal research to create discrete neuroanatomical lesions. For example, it has been used to lesion the basal forebrain nuclei to create a putative animal model of Alzheimer s disease (Arbogast and Kozlowski 1988). 

The aim of this chapter is to highlight recent advances in fractionation techniques for grape seed PAs, using as examples methods we are using for large-scale fractionation into monomers, oligomers, and polymers for assessment of bioactivity and bioavailability in animal model studies of Alzheimer s disease. Our methods represent modifications/combinations of previously described approaches. We first discuss the available methods and modifications and then present a case study for the fractionation of MegaNatural-AZ GSE. 

Moreover, all cells are not equally targeted in Alzheimer s disease, a disease that has discernable effects on consciousness (Perry et al., 1999). Large pyramidal cells of the frontal and temporal cortex, as well as the large pyramidal cells in CAl of hippocampus and subiculum, are the most susceptible to develop neurofibrillary tangles, to become dysfunctional and ultimately to die (Mann, 1996). It is the accumulation of abnormally hyperphosphorylated tau that disrupts the microtubular system of pyramidal cells in cortex and hippocampus both in experimental animal models and in Alzheimer s disease brain (Gong et al., 2000). 

Myriad Genetics reports that Flurizan is a selective amyloid-lowering agent (SALA) that reduces levels of the peptide amyloid beta 43 in cultured human cells and in animal models. Results of a completed Phase II follow-on study of Flurizan in patients with mild AD were presented in July 2006 at the International Conference on Alzheimer s Disease and Related Disorders. According to Myriad Genetics, results from this study reportedly... 

---