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fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Languages: English
Types: Doctoral thesis
Subjects: BF, RC0321
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder for which there is no cure. At the neuropathological level, AD is characterized by the presence of large numbers of amyloid-beta containing plaques (Aβ-plaques), and neurofibrillary tangles\ud comprised mostly of hyperphosphorylated aggregated protein tau. Both types of deposit are associated with neuroinflammation, synaptic and neuronal cell loss.\ud Accumulating evidence indicates a role for metabolic dysfunction in the pathogenesis of AD. Type 2 diabetes increases the risk of developing AD and several post-mortem\ud analyses have reported evidence of insulin resistance in Alzheimer brain tissue. \ud Insulin-based therapies have emerged as potential strategies to slow cognitive decline in AD, these include the use of insulin sensitizers, such as rosiglitazone, which mediates its effects on insulin sensitivity via the peroxisome proliferator-activated receptors-gamma (PPAR-γ) receptor. While the results of insulin sensitizers on\ud cognition in animal models of AD have been largely positive, the impact of these compounds on cognitive decline in AD patients has been variable.\ud Animal experiments provide a unique opportunity to examine the specific conditions and mechanisms by which insulin sensitizer’s impact on AD-related pathology. This thesis details experiments conducted in a popular Amyloid Precursor\ud Protein overexpressing transgenic mouse model of amyloid pathology that overproduces human Aβ. The aim of these experiments was to determine if chronic dosing with rosiglitazone ameliorated phenotypic behavioural deficits in transgenic mice, and lowered specific biomarkers associated with Aβ over-production. The results indicate that rosiglitazone largely does not reverse phenotypic behavioural alterations in these mice, nor does it reduce total Aβ levels. From this preclinical data, it is concluded that rosiglitazone is likely not a suitable therapeutic treatment for use in human patients with AD.
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    • 24(45): p. 10191-200.
    • Gong, Y., et al., Alzheimer's disease-affected brain: presence of oligomeric A beta ligands (ADDLs) suggests a molecular basis for reversible memory loss. Proc Natl Acad Sci U S A, 2003. 100(18): p.
    • Kotilinek, L.A., et al., Reversible memory loss in a mouse transgenic model of Alzheimer's disease. J Neurosci, 2002. 22(15): p. 6331-5.
    • Chang, L., et al., Femtomole immunodetection of synthetic and endogenous amyloid-beta oligomers and its application to Alzheimer's disease drug candidate screening. J Mol Neurosci, 2003. 20(3): p. 305-13.
    • Wu, Y., et al., Amyloid-beta-induced pathological behaviors are suppressed by Ginkgo biloba extract EGb 761 and ginkgolides in transgenic Caenorhabditis elegans. J Neurosci, 2006. 26(50): p. 13102-13.
    • Leon, W.C., et al., A novel transgenic rat model with a full Alzheimer's-like amyloid pathology displays pre-plaque intracellular amyloid-beta-associated cognitive impairment. J Alzheimers Dis, 2010. 20(1): p.
    • Conde, J.R. and W.J. Streit, Microglia in the aging brain. J Neuropathol Exp Neurol, 2006. 65(3): p. 199- 203.
    • Norden, D.M. and J.P. Godbout, Microglia of the Aged Brain: Primed to be Activated and Resistant to Regulation. Neuropathol Appl Neurobiol, 2012.
    • Henry, C.J., Role of Primed Microglia in the Aging Brain in Prolonged Sickness and Depressive Behavior Concomitant with Peripheral Immune Stimulation, in Graduate School of The Ohio State University2011, The Ohio State University: Ohio, USA. p. 185.
    • Chiovenda, P., G.M. Vincentelli, and F. Alegiani, Cognitive impairment in elderly ED patients: need for multidimensional assessment for better management after discharge. Am J Emerg Med, 2002. 20(4): p.
    • Wofford, J.L., L.R. Loehr, and E. Schwartz, Acute cognitive impairment in elderly ED patients: etiologies and outcomes. Am J Emerg Med, 1996. 14(7): p. 649-53.
    • Streit, W.J., Microglial senescence: does the brain's immune system have an expiration date? Trends Neurosci, 2006. 29(9): p. 506-10.
    • Holmes, C., Systemic inflammation and Alzheimer's Disease. Neuropathol Appl Neurobiol, 2012.
    • Holmes, C. and J. Butchart, Systemic inflammation and Alzheimer's disease. Biochem Soc Trans, 2011.
    • 39(4): p. 898-901.
    • Streit, W.J. and Q.S. Xue, Alzheimer's disease, neuroprotection, and CNS immunosenescence. Front Pharmacol, 2012. 3: p. 138.
    • Mrak, R.E., Microglia in Alzheimer brain: a neuropathological perspective. Int J Alzheimers Dis, 2012.
    • 2012: p. 165021.
    • Bhat, R., et al., Astrocyte senescence as a component of Alzheimer's disease. PLoS One, 2012. 7(9): p.
    • e45069.
    • Campisi, J., Cellular senescence: putting the paradoxes in perspective. Curr Opin Genet Dev, 2011.
    • 21(1): p. 107-12.
    • Raji, M.A., et al., Effect of a dementia diagnosis on survival of older patients after a diagnosis of breast, colon, or prostate cancer: implications for cancer care. Arch Intern Med, 2008. 168(18): p. 2033-40.
    • Attner, B., et al., Low cancer rates among patients with dementia in a population-based register study in Sweden. Dement Geriatr Cogn Disord, 2010. 30(1): p. 39-42.
    • Markesbery, W.R. and J.M. Carney, Oxidative alterations in Alzheimer's disease. Brain Pathol, 1999.
    • 9(1): p. 133-46.
    • Massaad, C.A. and E. Klann, Reactive oxygen species in the regulation of synaptic plasticity and memory. Antioxid Redox Signal, 2011. 14(10): p. 2013-54.
    • Zhu, X., et al., Causes of oxidative stress in Alzheimer disease. Cell Mol Life Sci, 2007. 64(17): p. 2202- 10.
    • Bonda, D.J., et al., Role of metal dyshomeostasis in Alzheimer's disease. Metallomics, 2011. 3(3): p. 267- 70.
    • Watt, N.T., I.J. Whitehouse, and N.M. Hooper, The role of zinc in Alzheimer's disease. Int J Alzheimers Dis, 2010. 2011: p. 971021.
    • Olanow, C.W., An introduction to the free radical hypothesis in Parkinson's disease. Ann Neurol, 1992.
    • 32 Suppl: p. S2-9.
    • Huang, X., et al., Redox-active metals, oxidative stress, and Alzheimer's disease pathology. Ann N Y Acad Sci, 2004. 1012: p. 153-63.
    • CNS Neurosci Ther, 2011. 17(4): p. 256-68.
    • Mantyh, P.W., et al., Aluminum, iron, and zinc ions promote aggregation of physiological concentrations of beta-amyloid peptide. J Neurochem, 1993. 61(3): p. 1171-4.
    • Bush, A.I., et al., Rapid induction of Alzheimer A beta amyloid formation by zinc. Science, 1994.
    • 265(5177): p. 1464-7.
    • Bush, A.I., et al., The amyloid beta-protein precursor and its mammalian homologues. Evidence for a zinc-modulated heparin-binding superfamily. J Biol Chem, 1994. 269(43): p. 26618-21.
    • Rottkamp, C.A., et al., Redox-active iron mediates amyloid-beta toxicity. Free Radic Biol Med, 2001.
    • 30(4): p. 447-50.
    • Lovell, M.A., et al., Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci, 1998.
    • 158(1): p. 47-52.
    • Acta Neuropathol, 1990. 81(2): p. 105-10.
    • De Felice, F.G., et al., Abeta oligomers induce neuronal oxidative stress through an N-methyl-Daspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. J Biol Chem, 2007. 282(15): p. 11590-601.
    • Andorn, A.C. and R.N. Kalaria, Factors Affecting Pro- and Anti-Oxidant Properties of Fragments of the b-Protein Precursor (bPP): Implication for Alzheimer's Disease. J Alzheimers Dis, 2000. 2(2): p. 69-78.
    • Folia Neuropathol, 2001. 39(3): p. 163-73.
    • Yan, S.D., et al., Non-enzymatically glycated tau in Alzheimer's disease induces neuronal oxidant stress resulting in cytokine gene expression and release of amyloid beta-peptide. Nat Med, 1995. 1(7): p. 693-9.
    • Nunomura, A., et al., Neuronal oxidative stress precedes amyloid-beta deposition in Down syndrome. J Neuropathol Exp Neurol, 2000. 59(11): p. 1011-7.
    • Nunomura, A., et al., Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol, 2001. 60(8): p. 759-67.
    • Cuajungco, M.P., et al., Evidence that the β-Amyloid Plaques of Alzheimer's Disease Represent the Redox-silencing and Entombment of Aβ by Zinc. Journal of Biological Chemistry, 2000. 275(26): p.
    • Curtain, C.C., et al., Alzheimer's disease amyloid-beta binds copper and zinc to generate an allosterically ordered membrane-penetrating structure containing superoxide dismutase-like subunits. J Biol Chem, 2001. 276(23): p. 20466-73.
    • Panegyres, P.K., The effects of excitotoxicity on the expression of the amyloid precursor protein gene in the brain and its modulation by neuroprotective agents. J Neural Transm, 1998. 105(4-5): p. 463-78.
    • Lee, H.G., et al., Amyloid-beta in Alzheimer disease: the null versus the alternate hypotheses. J Pharmacol Exp Ther, 2007. 321(3): p. 823-9.
    • Davis, D.G., et al., Alzheimer neuropathologic alterations in aged cognitively normal subjects. J Neuropathol Exp Neurol, 1999. 58(4): p. 376-88.
    • Supnet, C. and I. Bezprozvanny, The dysregulation of intracellular calcium in Alzheimer disease. Cell Calcium, 2010. 47(2): p. 183-9.
    • Takahashi, M., et al., Amyloid precursor proteins inhibit heme oxygenase activity and augment neurotoxicity in Alzheimer's disease. Neuron, 2000. 28(2): p. 461-73.
    • Smith, M.A., et al., Widespread peroxynitrite-mediated damage in Alzheimer's disease. J Neurosci, 1997.
    • 17(8): p. 2653-7.
    • Good, P.F., et al., Evidence of neuronal oxidative damage in Alzheimer's disease. Am J Pathol, 1996.
    • 149(1): p. 21-8.
    • Colavitti, R. and T. Finkel, Reactive oxygen species as mediators of cellular senescence. IUBMB Life, 2005. 57(4-5): p. 277-81.
    • Zhu, X., et al., Alzheimer disease, the two-hit hypothesis: an update. Biochim Biophys Acta, 2007.
    • 1772(4): p. 494-502.
    • de la Monte, S.M., Insulin resistance and Alzheimer's disease. BMB Rep, 2009. 42(8): p. 475-81.
    • Liao, F.F. and H. Xu, Insulin signaling in sporadic Alzheimer's disease. Sci Signal, 2009. 2(74): p. pe36.
    • Schioth, H.B., et al., Brain Insulin Signaling and Alzheimer's Disease: Current Evidence and Future Directions. Mol Neurobiol, 2011.
    • Zhao, W.Q. and M. Townsend, Insulin resistance and amyloidogenesis as common molecular foundation for type 2 diabetes and Alzheimer's disease. Biochim Biophys Acta, 2009. 1792(5): p. 482-96.
    • Banks, W.A., J.B. Owen, and M.A. Erickson, Insulin in the brain: There and back again. Pharmacol Ther, 2012.
    • Olson, A.L., Regulation of GLUT4 and Insulin-Dependent Glucose Flux. ISRN Molecular Biology, 2012.
    • 2012: p. 12.
    • Pan, W. and A.J. Kastin, Interactions of IGF-1 with the blood-brain barrier in vivo and in situ.
    • Neuroendocrinology, 2000. 72(3): p. 171-8.
    • Curr Alzheimer Res, 2012. 9(1): p. 35-66.
    • Hopkins, D.F. and G. Williams, Insulin receptors are widely distributed in human brain and bind human and porcine insulin with equal affinity. Diabet Med, 1997. 14(12): p. 1044-50.
    • Zhao, W., et al., Brain insulin receptors and spatial memory. Correlated changes in gene expression, tyrosine phosphorylation, and signaling molecules in the hippocampus of water maze trained rats. J Biol Chem, 1999. 274(49): p. 34893-902.
    • Havrankova, J., J. Roth, and M. Brownstein, Insulin receptors are widely distributed in the central nervous system of the rat. Nature, 1978. 272(5656): p. 827-9.
    • Adolfsson, R., et al., Hypoglycemia in Alzheimer's disease. Acta Med Scand, 1980. 208(5): p. 387-8.
    • Schmitt, Editors. 1967, Rockefeller University Press: New York. p. .
    • Deng, W., J.B. Aimone, and F.H. Gage, New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory? Nat Rev Neurosci, 2010. 11(5): p. 339-50.
    • Lazarini, F. and P.M. Lledo, Is adult neurogenesis essential for olfaction? Trends Neurosci, 2011. 34(1): p. 20-30.
    • Galvan, V. and K. Jin, Neurogenesis in the aging brain. Clin Interv Aging, 2007. 2(4): p. 605-10.
    • Neuron, 2009. 64(1): p. 79-92.
    • Baskin, D.G., et al., Regional concentrations of insulin in the rat brain. Endocrinology, 1983. 112(3): p.
    • Das, P., et al., Electrophysiological and behavioral phenotype of insulin receptor defective mice. Physiol Behav, 2005. 86(3): p. 287-96.
    • Schubert, M., et al., Role for neuronal insulin resistance in neurodegenerative diseases. Proc Natl Acad Sci U S A, 2004. 101(9): p. 3100-3105.
    • Fisher, S.J., et al., Insulin Signaling in the Central Nervous System Is Critical for the Normal Sympathoadrenal Response to Hypoglycemia. Diabetes, 2005. 54(5): p. 1447-1451.
    • Blakesley, V.A., et al., Signaling via the insulin-like growth factor-I receptor: does it differ from insulin receptor signaling? Cytokine Growth Factor Rev, 1996. 7(2): p. 153-9.
    • Nature, 2001. 414(6865): p. 799-806.
    • Magarinos, A.M. and B.S. McEwen, Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress. Proc Natl Acad Sci U S A, 2000. 97(20): p. 11056-61.
    • Gispen, W.H. and G.J. Biessels, Cognition and synaptic plasticity in diabetes mellitus. Trends Neurosci, 2000. 23(11): p. 542-9.
    • Lupien, S.B., E.J. Bluhm, and D.N. Ishii, Systemic insulin-like growth factor-I administration prevents cognitive impairment in diabetic rats, and brain IGF regulates learning/memory in normal adult rats. J Neurosci Res, 2003. 74(4): p. 512-523.
    • Lang, B.T., et al., Impaired neurogenesis in adult type-2 diabetic rats. Brain Res, 2009. 1258: p. 25-33.
    • Stranahan, A.M., et al., Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons. Nat Neurosci, 2008. 11(3): p. 309-17.
    • Andrews, R.C. and B.R. Walker, Glucocorticoids and insulin resistance: old hormones, new targets. Clin Sci (Lond), 1999. 96(5): p. 513-23.
    • Qi, D. and B. Rodrigues, Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism. Am J Physiol Endocrinol Metab, 2007. 292(3): p. E654-67.
    • Reynolds, R.M. and B.R. Walker, Human insulin resistance: the role of glucocorticoids. Diabetes Obes Metab, 2003. 5(1): p. 5-12.
    • Siminialayi, I.M. and P.C. Emem-Chioma, Glucocorticoids and the insulin resistance syndrome. Niger J Med, 2004. 13(4): p. 330-5.
    • Teelucksingh, S., et al., Does insulin resistance co-exist with glucocorticoid resistance in the metabolic syndrome? Studies comparing skin sensitivity to glucocorticoids in individuals with and without acanthosis nigricans. Cardiovasc Diabetol, 2012. 11: p. 31.
    • Pomara, N., et al., Therapeutic implications of HPA axis abnormalities in Alzheimer's disease: review and update. Psychopharmacol Bull, 2003. 37(2): p. 120-34.
    • Huang, C.-W., et al., Elevated basal cortisol level predicts lower hippocampal volume and cognitive decline in Alzheimer's disease. Journal of Clinical Neuroscience, 2009. 16(10): p. 1283-1286.
    • Lupien, S.J., et al., Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nat Neurosci, 1998. 1(1): p. 69-73.
    • Huang, S.J., et al., Increase of insulin sensitivity and reversal of age-dependent glucose intolerance with inhibition of ASIC3. Biochem Biophys Res Commun, 2008. 371(4): p. 729-34.
    • Lamport, D.J., et al., Impairments in glucose tolerance can have a negative impact on cognitive function: A systematic research review. Neuroscience & Biobehavioral Reviews, 2009. 33(3): p. 394-413.
    • Nooyens, A.C., et al., Type 2 diabetes and cognitive decline in middle-aged men and women: the Doetinchem Cohort Study. Diabetes Care, 2010. 33(9): p. 1964-9.
    • Williamson, R., A. McNeilly, and C. Sutherland, Insulin resistance in the brain: an old-age or new-age problem? Biochem Pharmacol, 2012. 84(6): p. 737-45.
    • Allen, K.V., B.M. Frier, and M.W. Strachan, The relationship between type 2 diabetes and cognitive dysfunction: longitudinal studies and their methodological limitations. Eur J Pharmacol, 2004. 490(1-3): p. 169-75.
    • Samaras, K. and P.S. Sachdev, Diabetes and the elderly brain: sweet memories? Ther Adv Endocrinol Metab, 2012. 3(6): p. 189-96.
    • Trial., T.D.C.a.C., Long-Term Effect of Diabetes and Its Treatment on Cognitive Function. New England Journal of Medicine, 2007. 356(18): p. 1842-1852.
    • Swaab, D.F., et al., Increased cortisol levels in aging and Alzheimer's disease in postmortem cerebrospinal fluid. J Neuroendocrinol, 1994. 6(6): p. 681-7.
    • Lee, H.K., et al., The insulin/Akt signaling pathway is targeted by intracellular beta-amyloid. Mol Biol Cell, 2009. 20(5): p. 1533-44.
    • Greenfield, J.P., et al., Cellular and molecular basis of beta-amyloid precursor protein metabolism. Front Biosci, 2000. 5: p. D72-83.
    • Saavedra, L., et al., Internalization of beta-amyloid peptide by primary neurons in the absence of apolipoprotein E. J Biol Chem, 2007. 282(49): p. 35722-32.
    • Ott, A., et al., Diabetes mellitus and the risk of dementia: The Rotterdam Study. Neurology, 1999. 53(9): p. 1937-42.
    • Aisen, P.S. and B. Vellas, Editorial: passive immunotherapy for Alzheimer's disease: what have we learned, and where are we headed? J Nutr Health Aging, 2013. 17(1): p. 49-50.
    • Sarafidis, P.A., Thiazolidinedione derivatives in diabetes and cardiovascular disease: an update. Fundam Clin Pharmacol, 2008. 22(3): p. 247-64.
    • Heneka, M.T. and G.E. Landreth, PPARs in the brain. Biochim Biophys Acta, 2007. 1771(8): p. 1031-45.
    • Yki-Jarvinen, H., Thiazolidinediones. N Engl J Med, 2004. 351(11): p. 1106-18.
    • Xu, H., et al., Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest, 2003. 112(12): p. 1821-30.
    • Mohanty, P., et al., Evidence for a potent antiinflammatory effect of rosiglitazone. J Clin Endocrinol Metab, 2004. 89(6): p. 2728-35.
    • Strum, J.C., et al., Rosiglitazone induces mitochondrial biogenesis in mouse brain. J Alzheimers Dis, 2007. 11(1): p. 45-51.
    • Neurotherapeutics, 2008. 5(3): p. 481-9.
    • Hyong, A., et al., Rosiglitazone, a PPAR gamma agonist, attenuates inflammation after surgical brain injury in rodents. Brain Res, 2008. 1215: p. 218-24.
    • Kaundal, R.K. and S.S. Sharma, Peroxisome proliferator-activated receptor gamma agonists as neuroprotective agents. Drug News Perspect, 2010. 23(4): p. 241-56.
    • Ramanan, S., et al., Role of PPARs in Radiation-Induced Brain Injury. PPAR Res, 2010. 2010: p.
    • Braissant, O., et al., Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat. Endocrinology, 1996. 137(1): p.
    • Willson, T.M., et al., The PPARs: from orphan receptors to drug discovery. J Med Chem, 2000. 43(4): p.
    • Free Radic Biol Med, 2009. 46(8): p. 989-1003.
    • Lehmann, J.M., et al., An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma). J Biol Chem, 1995. 270(22): p. 12953-6.
    • Hernandez, R., T. Teruel, and M. Lorenzo, Rosiglitazone produces insulin sensitisation by increasing expression of the insulin receptor and its tyrosine kinase activity in brown adipocytes. Diabetologia, 2003. 46(12): p. 1618-28.
    • Kramer, D., et al., Insulin-sensitizing effect of rosiglitazone (BRL-49653) by regulation of glucose transporters in muscle and fat of Zucker rats. Metabolism, 2001. 50(11): p. 1294-300.
    • Diabetes Care, 2005. 28(9): p. 2322-2325.
    • Arita, Y., et al., Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity. Biochem Biophys Res Commun, 1999. 257(1): p. 79-83.
    • Weyer, C., et al., Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab, 2001. 86(5): p. 1930-5.
    • Stefan, N., et al., Plasma Adiponectin Concentration Is Associated With Skeletal Muscle Insulin Receptor Tyrosine Phosphorylation, and Low Plasma Concentration Precedes a Decrease in Whole-Body Insulin Sensitivity in Humans. Diabetes, 2002. 51(6): p. 1884-1888.
    • Hotta, K., et al., Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients. Arterioscler Thromb Vasc Biol, 2000. 20(6): p. 1595-9.
    • Sepilian, V. and M. Nagamani, Adiponectin levels in women with polycystic ovary syndrome and severe insulin resistance. J Soc Gynecol Investig, 2005. 12(2): p. 129-34.
    • Carmina, E., et al., Evidence for altered adipocyte function in polycystic ovary syndrome. Eur J Endocrinol, 2005. 152(3): p. 389-94.
    • Gynecol Obstet Invest, 2005. 60(3): p. 155-61.
    • Ardawi, M.S. and A.A. Rouzi, Plasma adiponectin and insulin resistance in women with polycystic ovary syndrome. Fertil Steril, 2005. 83(6): p. 1708-16.
    • Yamauchi, T., et al., The Mechanisms by Which Both Heterozygous Peroxisome Proliferator-activated Receptor γ (PPARγ) Deficiency and PPARγ Agonist Improve Insulin Resistance. Journal of Biological Chemistry, 2001. 276(44): p. 41245-41254.
    • Maeda, N., et al., PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein. Diabetes, 2001. 50(9): p. 2094-9.
    • Tuepker, J., Effect of rosiglitazone treatment on nontraditional markers of cardiovascular disease in patients with type 2 diabetes mellitus. Circulation, 2003. 107(16): p. e109; author reply e109.
    • Diabetes Care, 2006. 29(1): p. 139-41.
    • Liao, W., et al., Adiponectin induces interleukin-6 production and activates STAT3 in adult mouse cardiac fibroblasts. Biol Cell, 2009. 101(5): p. 263-72.
    • Guzowski, J.F., J.J. Knierim, and E.I. Moser, Ensemble dynamics of hippocampal regions CA3 and CA1.
    • Neuron, 2004. 44(4): p. 581-4.
    • Biggs, D.S., 3D deconvolution microscopy. Curr Protoc Cytom, 2010. Chapter 12: p. Unit 12 19 1-20.
    • Rodriguez, A., et al., Automated three-dimensional detection and shape classification of dendritic spines from fluorescence microscopy images. PLoS One, 2008. 3(4): p. e1997.
    • Rodriguez, A., et al., Rayburst sampling, an algorithm for automated three-dimensional shape analysis from laser scanning microscopy images. Nat Protoc, 2006. 1(4): p. 2152-61.
    • Araki, W., et al., IGF-1 promotes beta-amyloid production by a secretase-independent mechanism.
    • Biochem Biophys Res Commun, 2009. 380(1): p. 111-4.
    • van Himbergen, T.M., et al., Biomarkers for insulin resistance and inflammation and the risk for allcause dementia and alzheimer disease: results from the Framingham Heart Study. Arch Neurol, 2012.
    • 69(5): p. 594-600.
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