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S performed using the ABC method, and revealed with DAB (brown precipitate)-see Experimental Procedures. Sections were lightly counterstained with Hematoxylin (blue) to help reveal the tissue architecture. Cerebellar layers: ml = molecular layer; pc = Purkinje cell layer; gc = granule cell layer; wm = white matter. Note focal pc loss in A2, and large zones of pc loss in A3 and A4. (Original Magni
Ingomyelin phosphodiesterase; SPTLC: Serine palmitoyltransferase; STZ: Streptozotocin; T2DM: Type 2 diabetes mellitus; TBS: Tris buffered saline; UGCG: UDP-glucose ceramide glycoysltransferase. Acknowledgements Supported by AA-11431, AA-12908, and K24-AA-16126 from the National Institutes of Health. Author details 1 Department of Pathology (Neuropathology), Rhode Island Hospital, 593 Eddy Street,
Ration have soared over the past several decades, suggesting that exposures rather than genetics dictate their etiologies. Our over-arching hypothesis is that shifts in lifestyles and economics have led us to chronically consume excess fat, and get exposed to agents that cause insulin resistance. Consideration given to potential pathogenic agents was focused by the experimental evidence showing t
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
P. Chronic HFD feeding aloneTable 3 Effects of High Fat Diet and NDEA Exposure on Biomarkers of Insulin and IGF Resistance in the CerebellummRNA AbPP Tau AChE ChAT Insulin IGF-1 IGF-2 Insulin R IGF-1R IGF-2R IRS-1 IRS-2 IRS-4 LFD+VEH 7.007 ?0.828 12.230 ?1.098 2.829 ?0.178 0.701 ?0.045 0.754 ?0.048 0.957 ?0.119 12.000 ?1.800 17.090 ?1.547 5.031 ?0.525 5.677 ?0.548 5.559 ?0.411 7.701 ?0.509 0.135
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
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
Antibody (1:10000) and Amplex Red soluble fluorophore [79]. Amplex Red fluorescence was measured (Ex 579/Em 595) in a SpectraMax M5 microplate reader (Molecular Devices Corp., Sunnyvale, CA). Negative control reactions included substitutions with nonrelevant primary or secondary antibodies, and omission of primary or secondary antibody. Immunoreactivities were normalized to protein content as det
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
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
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
E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy
Ation with impairments in insulin/IGF signaling mechanisms, and deficits in cholinergic and neuronal cytoskeletal gene and protein expression in brain, whereas chronic HFD feeding alone produces more restrictive deficits in insulin/IGF signaling mechanisms with reduced ChAT expression and increased oxidative stress. The combined exposures caused overlapping structural and molecular abnormalities
Ation and glial cytoplasmic inclusions. Ann Neurol 1996, 39(2):241-255. 49. Burk K, Globas C, Wahl T, Buhring U, Dietz K, Zuhlke C, Luft A, Schulz JB, Voigt K, Dichgans J: MRI-based volumetric differentiation of sporadic cerebellar ataxia. Brain 2004, 127(Pt 1):175-181.50. Dickson DW, Lin W, Liu WK, Yen SH: Multiple system atrophy: a sporadic synucleinopathy. Brain Pathol 1999, 9(4):721-732. 51.
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