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S. Nutr Rev 2007, 65(12 Pt 2):S152-156. 2. Launer LJ: Next steps in Alzheimer's disease research: interaction between epidemiology and basic science. Curr Alzheimer Res 2007, 4(2):141-143. 3. Wang XP, Ding HL: Alzheimer's disease: epidemiology, genetics, and beyond. Neurosci Bull 2008, 24(2):105-109. 4. de la Monte SM, Neusner A, Chu J, Lawton M: Epidemilogical Trends Strongly Suggest Exposures a
We measured gene expression corresponding to insulin and IGF polypeptides and receptors, and insulin receptor substrates (IRSs) that transmit signals required for growth, survival, energy metabolism, and neuronalELISAs were used to measure sustained effects of NDEA treatment and/or chronic HFD feeding on Tau, phospho-Tau, AbPP, AbPP-Ab, ChAT, and AChE levels in brain tissue. Early limited exposur
Or NDEA-associated neurodegeneration and insulin/IGF resistance were likely mediated by increased brain ceramide levels. Those studies demonstrated strikingly increased expression of several genes regulating ceramide production via both de novo biosynthesis or sphingomyelin degradation pathways in NDEA-treated rats, irrespective of chronic HFD feeding. Since NDEA is lipid soluble [115,116] and ca
Terbalance the tendency of two other major neurotransmitters in the brain dopamine and noradrenaline to encourage overarousal, fear, anger, tension, aggression, violence, obsessive-compulsive actions, overeating, anxiety and sleep disturbances [60].Page 8 of(page number not for citation purposes)BMC Physiology 2009, 9:http://www.biomedcentral.com/1472-6793/9/ConclusionThe present results revealed
Al microenvironment. Cell Cycle. 2010;9(17):3515?3. 56. Martinez-Outschoorn UE, Balliet RM, Rivadeneira DB, Chiavarina B, Pavlides S, Wang C, et al. Oxidative stress in cancer associated fibroblasts drives tumorstroma co-evolution: A new paradigm for understanding tumor metabolism, the field effect and genomic instability in cancer cells. Cell Cycle. 2010;9(16):3256?6. 57. Chiavarina B, Whitaker-
Enile plaques of Alzheimer's disease. Acta Neuropathol 1990, 79(5):486-493.Tong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 15 of71. Baloyannis SJ: Dendritic pathology in Alzheimer's disease. J Neurol Sci 2009, 283(1-2):153-157. 72. Baloyannis SJ, Manolidis SL, Manolidis LS: Synaptic alterations in the vestibulocerebellar system in Alzheimer's disease
S, could result in cytoskeletal collapse and synaptic disconnection. Alternatively, the finding could reflect neuronal loss associated with neurodegeneration. The reduced levels of ChAT reflect deficits in acetylcholine homeostasis that contribute to cognitive impairment with neurodegeneration [101,102]. Correspondingly, in preliminary studies, we detected evidence of significant spatial learning
N in ways that could cause insulin/IGF resistance in the brain, their specific effects were not identical. The main effect of NDEA, with or without HFD feeding, was to reduce mRNA levels of insulin receptor, IGF-2 receptor, and IRS-2, which would have impaired signaling at the receptor level, and downstream through IRS-2, one of main docking proteins responsible for transmitting survival, growth,
R palsy. J Neuropathol Exp Neurol 2001, 60(5):403-410. 64. Rusina R, Bourdain F, Matej R: [Multiple system atrophy and Alzheimer's disease: a case report of a rare association of two neuro-degenerative disorders]. Rev Neurol (Paris) 2007, 163(12):1239-1241. 65. Engel PA, Grunnet M: Atypical dementia and spastic paraplegia in a patient with primary lateral sclerosis and numerous necortical beta am
Changes characterized by focal loss of Purkinje neurons (Fig. 1-A3). NDEA exposure, with or without chronic HFD feeding, resulted in loss of Purkinje cells (Figs. 1-A2, 1-A4) and variable thinning of the granule cell layer. Immunohistochemical staining demonstrated similar levels and distributions of GFAP immunoreactivity in cells distributed in the granule layer of control (Fig 1-B1) and HFD-fed
Xidative stress and neurodegeneration. Cerebellar protein homogenates were used to measure (A) GSK-3b; (B) phospho (p)-GSK-3b; (C) GFAP; (D) GAPDH; (E) HNE; (F) malondialdehyde, MDA; (G) Nitrotyrosine, N-TYR; or (H) b-Actin; by direct binding ELISA. Immunoreactivity was detected with HRP-conjugated secondary antibody and Amplex Red soluble fluorophor. Fluorescence light units (FLU) were measured
Ki M, Kitagaki H, Yamaji S, Sakamoto S, Matsuda K, Mori E: Reduction of cerebellar glucose metabolism in advanced Alzheimer's disease. J Nucl Med 1997, 38(6):925-928. 58. Larner AJ: The cerebellum in Alzheimer's disease. Dement Geriatr Cogn Disord 1997, 8(4):203-209. 59. Wegiel J, Wisniewski HM, Dziewiatkowski J, Badmajew E, Tarnawski M, Reisberg B, Mlodzik B, De Leon MJ, Miller DC: Cerebellar at
R protein; AbPP-Ab: amyloid-b peptide; AChE: acetylcholinesterase; AD: Alzheimer's disease; CER: Ceramide synthase; ChAT: choline acetyltransferase; ELISA: enzyme-linked immunosorbant assay; GFAP: glial fibrillary acidic protein; GSK-3b: glycogen synthase kinase-3b; H E: hematoxylin and eosin; HFD: high fat diet; HNE: 4-hydroxy-2-nonenal; HRP: horseradish peroxidase; i.p.: intraperitoneal; IGF: I
Xidative stress and neurodegeneration. Cerebellar protein homogenates were used to measure (A) GSK-3b; (B) phospho (p)-GSK-3b; (C) GFAP; (D) GAPDH; (E) HNE; (F) malondialdehyde, MDA; (G) Nitrotyrosine, N-TYR; or (H) b-Actin; by direct binding ELISA. Immunoreactivity was detected with HRP-conjugated secondary antibody and Amplex Red soluble fluorophor. Fluorescence light units (FLU) were measured

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