(919) 237-4897 info@t3dtherapeutics.com

References

  1. Heininger K, (2000) A unifying hypothesis of Alzheimer’s disease. IV. Causation and sequence of events. Rev Neurosci. 11: Spec No: 213-328
  2. Yin, F., Boveris, A., and Cadenas, E. (2014). Mitochondrial energy metabolism and redox signaling in brain aging and neurodegeneration. Antioxid. Redox Signal. 20, 353–371.
  3. Lourenço CF, Ledo A, Dias C, Barbosa RM, Laranjinha J. Neurovascular and neurometabolic derailment in aging and Alzheimer’s disease. (2015) Frontiers in Aging Neuroscience. 7:103.
  4. de la Monte SM, Wands JR (2008) Alzheimer’s disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol 2: 1101-1113.
  5. Steen E, Terry BM, Rivera EJ, Cannon JL, Neely TR, et al. (2005) Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease–is this type 3 diabetes? J Alzheimers Dis 7: 63-80.
  6. Sato N, Morishita R. (2015) The roles of lipid and glucose metabolism in modulation of β-amyloid, tau, and neurodegeneration in the pathogenesis of Alzheimer disease. Frontiers in Aging Neuroscience. 7:199.
  7. Zlokovic BV. (2008) The blood-brain barrier in health and chronic neurodegenerative disorders. Neuron. 57:178–201.
  8. Hoyer S. (1998)  Is sporadic Alzheimer disease the brain type of non–insulin dependent diabetes mellitus? A challenging hypothesis. J Neural Transm. 105(4–5):415–422.
  9. Iwangoff P, Armbruster R, Enz A, Meier-Ruge W. (1980) Glycolytic enzymes from human autoptic brain cortex: normal aged and demented cases. Mech Ageing Dev. 14(1-2):203–9.
  10. Sims NR, et.al. (1980) Glucose metabolism and acetylcholine synthesis in relation to neuronal activity in Alzheimer’s disease. Lancet. 1(8164):333–6.
  11. Tong M, Deochand C, Didsbury J, de la Monte SM (2016) T3D-959: A Multi-Faceted Disease Remedial Drug Candidate for the Treatment of Alzheimer’s Disease. J Alzheimers Dis 51, 123-138.
  12. Tong M, Dominguez C, Didsbury J, de la Monte SM (2016) Targeting Alzheimer’s Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies. J Alzheimers Dis Parkinsonism 6: 238. doi: 10.4172/2161- 0460.1000238.
  13. http://www.ddw-online.com/therapeutics/p213493-targeting-diminished-cerebral-glucose-metabolism-for-alzheimer%E2%80%99s-disease-summer-13.html
  14. Chen Z, Zhong C. (2013) Decoding Alzheimer’s disease from perturbed cerebral glucose metabolism: Implications for diagnostic and therapeutic strategies. Progress in Neurobiology 108:21-43.
  15. Iwashita A. et.al. (2007) Neuroprotective efficacy of the peroxisome proliferator-activated receptor delta-selective agonists in vitro and in vivo. J Pharmacol. Exp. Ther. 320:1087-1096.
  16. Bright, JJ, et al. (2008) PPAR regulation of inflammatory signaling in CNS diseases, PPAR Research. Article ID 658520, doi:10.1155/2008/658520.
  17. de la Monte SM, et.al. (2006) Therapeutic rescue of neurodegeneration in experimental type 3 diabetes: relevance to Alzheimer’s disease. J Alzheimers Dis. 10(1):89–109.
  18. Fortress AM, et al. (2013) Canonical Wnt Signaling is Necessary for Object Recognition Memory Consolidation. Journal of Neuroscience. 33 (31): 12619-26.
  19. Inestosa NC and Toledo EM. (2008) The role of Wnt signaling in neuronal dysfunction in Alzheimer’s Disease. Mol Neurodegener. 3:3-9.
  20. Scholtysek, C, et.al. (2013) PPARβ/δ governs Wnt signaling and bone turnover, Nature Medicine. 19:608-13.
  21. Kummer, MP and Heneka MT. (2008) PPARs in Alzheimer’s Disease, PPAR Research. Article ID 403896;
  22. Kalinin, S. et.al. (2009) A PPAR delta agonist reduces amyloid burden and brain inflammation in a transgenic mouse model of Alzheimer’s disease. Curr. Alzheimer Res. 6(5):431-7.
  23. Barroso E, Santos A,, Porquet D, Del Valle J, Michalik L, Wahli W, Vázquez-Carrera M. (2012) Peroxisome Proliferator-Activated Receptor Beta/Delta-Deficient Mice Show Increased Inflammation And Tau Phosphorylation In Cortex. FENS Abstract. 6:p044.28.
  24. Dunn SE, Bhat R, Straus DS, Sobel RA, Axtell R, et al. (20100 Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity.  J Exp Med. 207:1599–1608.
  25. Tokutake T, et al. (2012) Hyperphosphorylation of Tau induced by naturally secreted amyloid-β at nanomolar concentrations is modulated by insulin-dependent Akt-GSK3β signaling pathway J Biol Chem. 287(42):35222-33).
  26. Grady CL, Haxby JV, Schlageter NL, Berg G, Rapoport SI (1986) Stability of metabolic and neuropsychological asymmetries in dementia of the Alzheimer type. Neurology 36: 1390-1392.
  27. Mosconi L (2005) Brain glucose metabolism in the early and specific diagnosis of Alzheimer’s disease. FDG-PET studies in MCI and AD. Eur J Nucl Med Mol Imaging 32: 486-510.
  28. Mosconi L, McHugh PF (2011) FDG- and amyloid-PET in Alzheimer’s disease: Is the whole greater than the sum of the parts? Q J Nucl Med Mol Imaging 55: 250-264.
  29. Brown AM, Sheu RK, Mohs R, Haroutunian V, Blass JP (2001) Correlation of the clinical severity of Alzheimer’s disease with an aberration in mitochondrial DNA (mtDNA). J Mol Neurosci 16: 41-48.
  30. Arnaiz E, et al. (2001) Impaired cerebral glucose metabolism and cognitive functioning predict deterioration in mild cognitive impairment. Neuroreport. 12(4):851-5.
  31. Landau SM, Harvey D, Madison CM, et al. (2011) Associations between cognitive, functional, and FDG-PET measures of decline in AD and MCI. Neurobiol Aging. 32(7):1207-18.
  32. Alexander GE, Chen K, Pietrini P, Rapoport SI, Reiman EM (2002) Longitudinal PET evaluation of cerebral metabolic decline in dementia: a potential outcome measure in Alzheimer’s disease treatment studies. Am J Psychiatry. 159:738–745.
  33. Engler H, Forsberg A, Almkvist O, et al. (2006) Two-year follow-up of amyloid deposition in patients with Alzheimer’s disease. Brain. 129:2856–2866.
  34. Dickey, A.S., Pineda, V.V., Tsunemi, T., Liu, P.P., Miranda, H.C., Gilmore-Hall, S.K., Lomas, N., Sampat, K.R., Buttgereit, A., Torres, M.J. et al. (2016) PPAR-delta is repressed in Huntington’s disease, is required for normal neuronal function and can be targeted therapeutically. Nat Med, 22, 37-45.