PGC-1α expression decreases in the Alzheimer disease brain as a function of dementia

Archives of Neurology

Volumn 66, Issue 3, 2009, Pages 352-361

  Qin, Weiping ^a   Haroutunian, Vahram ^a   Katsel, Pavel ^a   Cardozo, Christopher P ^a   Ho, Lap ^a,b,c   Buxbaum, Joseph D ^a   Pasinetti, Giulio M ^a,b,c  

^a MOUNT SINAI SCHOOL OF MEDICINE   (United States)

^b GERIATRIC RESEARCH EDUCATION AND CLINICAL CENTER   (United States)

^c VETERANS AFFAIRS MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA SECRETASE; AMYLOID BETA PROTEIN[1-40]; AMYLOID BETA PROTEIN[1-42]; FORKHEAD TRANSCRIPTION FACTOR; FORKHEAD TRANSCRIPTION FACTOR 1; GENE PRODUCT; MESSENGER RNA; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA COACTIVATOR 1ALPHA; UNCLASSIFIED DRUG; AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN (1 42); AMYLOID BETA-PROTEIN (1-42); AMYLOID PRECURSOR PROTEIN; FOXO3 PROTEIN, MOUSE; GLUCOSE; GREEN FLUORESCENT PROTEIN; HEAT SHOCK PROTEIN; PEPTIDE FRAGMENT; PPARGC1A PROTEIN, HUMAN; SECRETASE; TRANSCRIPTION FACTOR;

ALZHEIMER DISEASE; ANIMAL CELL; ARTICLE; BRAIN FUNCTION; CASE CONTROL STUDY; CONTROLLED STUDY; DEMENTIA; DISEASE COURSE; DNA MICROARRAY; ENZYME ACTIVITY; GENOME; GLUCOSE HOMEOSTASIS; HUMAN; HUMAN TISSUE; HYPERGLYCEMIA; MOUSE; NEUROPATHOLOGY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; REAL TIME POLYMERASE CHAIN REACTION; ANIMAL; ANIMAL EMBRYO; CELL CULTURE; CHEMISTRY; CULTURE MEDIUM; DOSE RESPONSE; DOWN REGULATION; DRUG EFFECT; GENE EXPRESSION PROFILING; GENETIC TRANSFECTION; GENETICS; HIPPOCAMPUS; METABOLISM; METHODOLOGY; NERVE CELL; PATHOLOGY; PHYSIOLOGY; TRANSGENIC MOUSE;

ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN; AMYLOID BETA-PROTEIN PRECURSOR; AMYLOID PRECURSOR PROTEIN SECRETASES; ANIMALS; CASE-CONTROL STUDIES; CELLS, CULTURED; CULTURE MEDIA, CONDITIONED; DEMENTIA; DISEASE PROGRESSION; DOSE-RESPONSE RELATIONSHIP, DRUG; DOWN-REGULATION; EMBRYO, MAMMALIAN; FORKHEAD TRANSCRIPTION FACTORS; GENE EXPRESSION PROFILING; GLUCOSE; GREEN FLUORESCENT PROTEINS; HEAT-SHOCK PROTEINS; HIPPOCAMPUS; HUMANS; MICE; MICE, TRANSGENIC; NEURONS; OLIGONUCLEOTIDE ARRAY SEQUENCE ANALYSIS; PEPTIDE FRAGMENTS; RNA, MESSENGER; TRANSCRIPTION FACTORS; TRANSFECTION;

EID: 62449166389     PISSN: 00039942     EISSN: 15383687     Source Type: Journal    
DOI: 10.1001/archneurol.2008.588     Document Type: Article

References (60)

1. Roberson ED, Mucke L. 100 Years and counting: prospects for defeating Alzheimer's disease. Science. 2006;314(5800):781-784.
2. Frölich L, Blum-Degen D, Bernstein HG, et al. Brain insulin and insulin receptors in aging and sporadic Alzheimer's disease. J Neural Transm. 1998;105(4-5):423-438.
3. Gerozissis K, Rouch C, Lemierre S, Nicolaidis S, Orosco M. A potential role of central insulin in learning and memory related to feeding. Cell Mol Neurobiol. 2001;21(4):389-401.
4. Jagust WJ, Seab JP, Huesman RH, et al. Diminished glucose transport in Alzheimer's disease: dynamic PET studies. J Cereb Blood Flow Metab. 1991;11(2):323-330.
5. Minoshima S, Frey KA, Foster NL, Kuhl DE. Preserved pontine glucose metabolism in Alzheimer disease: a reference region for functional brain image (PET) analysis. J Comput Assist Tomogr. 1995;19(4):541-547.
6. Hoyer S. Brain glucose and energy metabolism abnormalities in sporadic Alzheimer disease. Causes and consequences: an update. Exp Gerontol. 2000;35(9-10):1363-1372.
7. Hoyer S. Causes and consequences of disturbances of cerebral glucose metabolism in sporadic Alzheimer disease: therapeutic implications. Adv Exp Med Biol. 2004;541:135-152.
8. Craft S. Insulin resistance and Alzheimer's disease pathogenesis: potential mechanisms and implications for treatment. Curr Alzheimer Res. 2007;4(2):147-152.
9. Craft S. Insulin resistance syndrome and Alzheimer's disease: age- and obesity-related effects on memory, amyloid, and inflammation. Neurobiol Aging. 2005;26(1)(suppl 1):65-69.
10. Awad N, Gagnon M, Messier C. The relationship between impaired glucose tolerance, type 2 diabetes, and cognitive function. J Clin Exp Neuropsychol. 2004;26(8):1044-1080.
11. Craft S, Newcomer J, Kanne S, et al. Memory improvement following induced hyperinsulinemia in Alzheimer's disease. Neurobiol Aging. 1996;17(1):123-130.
12. Hoyer S. Abnormalities of glucose metabolism in Alzheimer's disease. Ann N Y Acad Sci. 1991;640:53-58.
13. Fukuyama H, Ogawa M, Yamauchi H, et al. Altered cerebral energy metabolism in Alzheimer's disease: a PET study. J Nucl Med. 1994;35(1):1-6.
14. Mielke R, Herholz K, Grond M, Kessler J, Heiss WD. Differences of regional cerebral glucose metabolism between presenile and senile dementia of Alzheimer type. Neurobiol Aging. 1992;13(1):93-98.
15. Herholz K, Schopphoff H, Schmidt M, et al. Direct comparison of spatially normalized PET and SPECT scans in Alzheimer's disease. J Nucl Med. 2002;43(1):21-26.
16. Henneberg N, Hoyer S. Desensitization of the neuronal insulin receptor: a new approach in the etiopathogenesis of late-onset sporadic dementia of the Alzheimer type (SDAT)? Arch Gerontol Geriatr. 1995;21(1):63-74.
17. de Leon MJ, Ferris SH, George AE, et al. Computed tomography and positron emission transaxial tomography evaluations of normal aging and Alzheimer's disease. J Cereb Blood Flow Metab. 1983;3(3):391-394.
18. Smith GS, de Leon MJ, George AE, et al. Topography of cross-sectional and longitudinal glucose metabolic deficits in Alzheimer's disease: pathophysiologic implications. Arch Neurol. 1992;49(11):1142-1150.
19. Hoyer S. Intermediary metabolism disturbance in AD/SDAT and its relation to molecular events. Prog Neuropsychopharmacol Biol Psychiatry. 1993;17(2):199-228.
20. Hoyer S. Glucose metabolism and insulin receptor signal transduction in Alzheimer disease. Eur J Pharmacol. 2004;490(1-3):115-125.
21. Small GW, Ercoli LM, Silverman DH, et al. Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease. Proc Natl Acad Sci U S A. 2000;97(11):6037-6042.
22. Reiman EM, Caselli RJ, Chen K, Alexander GE, Bandy D, Frost J. Declining brain activity in cognitively normal apolipoprotein E epsilon 4 heterozygotes: a foundation for using positron emission tomography to efficiently test treatments to prevent Alzheimer's disease. Proc Natl Acad Sci U S A. 2001;98(6):3334-3339.
23. Alexander GE, Chen K, Pietrini P, Rapoport SI, Reiman EM. Longitudinal PET evaluation of cerebral metabolic decline in dementia: a potential outcome measure in Alzheimer's disease treatment studies. Am J Psychiatry. 2002;159(5):738-745.
24. Haley AP, Knight-Scott J, Simnad VI, Manning CA. Increased glucose concentration in the hippocampus in early Alzheimer's disease following oral glucose ingestion. Magn Reson Imaging. 2006;24(6):715-720.
25. Puigserver P, Spiegelman BM. Peroxisome proliferator-activated receptorgamma coactivator 1 alpha (PGC-1 alpha): transcriptional coactivator and metabolic regulator. Endocr Rev. 2003;24(1):78-90.
26. Yoon JC, Puigserver P, Chen G, et al. Control of hepatic gluconeogenesis through the transcriptional coactivator PGC-1. Nature. 2001;413(6852):131-138.
27. Herzig S, Long F, Jhala US, et al. CREB regulates hepatic gluconeogenesis through the coactivator PGC-1. Nature. 2001;413(6852):179-183.
28. Puigserver P, Rhee J, Donovan J, et al. Insulin-regulated hepatic gluconeogenesis through FOXO1-PGC-1alpha interaction. Nature. 2003;423(6939):550-555.
29. Rhee J, Inoue Y, Yoon JC, et al. Regulation of hepatic fasting response by PPARγ coactivator-1α (PGC-1): requirement for hepatocyte nuclear factor 4α in gluconeogenesis. Proc Natl Acad Sci U S A. 2003;100(7):4012-4017.
30. Lin J, Wu PH, Tarr PT, et al. Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1α null mice. Cell. 2004;119(1):121-135.
31. Rodgers JT, Lerin C, Haas W, Gygi SP, Spiegelman BM, Puigserver P. Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature. 2005;434(7029):113-118.
32. Liang H, Ward WF. PGC-1alpha: a key regulator of energy metabolism. Adv Physiol Educ. 2006;30(4):145-151.
33. Tomlinson DR, Gardiner NJ. Glucose neurotoxicity. Nat Rev Neurosci. 2008;9(1):36-45.
34. Haroutunian V, Perl DP, Purohit DP, et al. Regional distribution of neuritic plaques in the nondemented elderly and subjects with very mild Alzheimer disease. Arch Neurol. 1998;55(9):1185-1191.
35. Davis KL, Mohs RC, Marin D, et al. Cholinergic markers in elderly patients with early signs of Alzheimer disease. JAMA. 1999;281(15):1401-1406.
36. Haroutunian V, Purohit DP, Perl DP, et al. Neurofibrillary tangles in nondemented elderly subjects and mild Alzheimer disease. Arch Neurol. 1999;56(6):713-718.
37. Haroutunian V, Davies PJ, Vianna C, Buxbaum JD, Purohit DP. Tau protein abnormalities associated with the progression of Alzheimer disease type dementia. Neurobiol Aging. 2007;28(1):1-7.
38. Mirra SS, Heyman A, McKeel D, et al. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD), part II: standardization of the neuropathologic assessment of Alzheimer's disease. Neurology. 1991;41(4):479-486.
39. Katsel P, Davis KL, Haroutunian V. Variations in myelin and oligodendrocyte-related gene expression across multiple brain regions in schizophrenia: a gene ontology study. Schizophr Res. 2005;79(2-3):157- 173.
40. Katsel P, Davis KL, Gorman JM, Haroutunian V. Variations in differential gene expression patterns across multiple brain regions in schizophrenia. Schizophr Res. 2005;77(2-3):241-252.
41. Katsel P, Li C, Haroutunian V. Gene expression alterations in the sphingolipid metabolism pathways during progression of dementia and Alzheimer's disease: a shift toward ceramide accumulation at the earliest recognizable stages of Alzheimer's disease? Neurochem Res. 2007;32(4-5):845-856.
42. Bolstad BM, Irizarry RA, Astrand M, Speed TP. A comparison of normalization methods for high density oligonucleotide array data based on variance and bias. Bioinformatics. 2003;19(2):185-193.
43. Irizarry RA, Hobbs B, Collin F, et al. Exploration, normalization, and summaries of high density oligonucleotide array probe level data. Biostatistics. 2003;4(2):249-264.
44. Klipper-Aurbach Y, Wasserman M, Braunspiegel-Weintrob N, et al. Mathematical formulae for the prediction of the residual beta cell function during the first two years of disease in children and adolescents with insulin-dependent diabetes mellitus. Med Hypotheses. 1995;45(5):486-490.
45. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. 2001;25(4):402-408.
46. Näslund J, Haroutunian V, Mohs R, et al. Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline. JAMA. 2000;283(12):1571-1577.
47. Kelley KA, Ho L, Winger D, et al. Potentiation of excitotoxicity in transgenic mice overexpressing neuronal cyclooxygenase-2. Am J Pathol. 1999;155(3):995-1004.
48. Skurk C, Maatz H, Kim HS, et al. The Akt-regulated forkhead transcription factor FoxO3a controls endothelial cell viability through modulation of the caspase-8 inhibitor FLIP. J Biol Chem. 2004;279(2):1513-1525.
49. Qin W, Ho L, Pompl PN, et al. Cyclooxygenase (COX)-2 and COX-1 potentiate beta-amyloid peptide generation through mechanisms that involve gamma-secretase activity. J Biol Chem. 2003;278(51):50970-50977.
50. Qin W, Yang T, Ho L, et al. Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction. J Biol Chem. 2006;281(31):21745-21754.
51. Burns M, Gaynor K, Olm V, et al. Presenilin redistribution associated with aberrant cholesterol transport enhances beta-amyloid production in vivo. J Neurosci. 2003;23(13):5645-5649.
52. Rezai-Zadeh K, Shytle D, Sun N, et al. Green tea epigallocatechin-3- gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice. J Neurosci. 2005;25(38):8807-8814.
53. Wang J, Ho L, Qin WP, et al. Caloric restriction attenuates beta-amyloid neuropathology in a mouse model of Alzheimer's disease. FASEB J. 2005;19(6):659-661.
54. Qin W, Chachich M, Lane M, et al. Calorie restriction attenuates Alzheimer's disease type brain amyloidosis in Squirrel monkeys (Saimiri sciureus). J Alzheimers Dis. 2006;10(4):417-422.
55. Sandri M, Lin J, Handschin C, et al. PGC-1alpha protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Proc Natl Acad Sci U S A. 2006;103(44):16260-16265.
56. Qin W, Zhao W, Ho L, et al. Regulation of forkhead transcription factor FoxO3a contributes to calorie restriction-induced prevention of Alzheimer's disease-type amyloid neuropathology and spatial memory deterioration. Ann N Y Acad Sci. 2008;1147:335-347.
57. Gandy S. Molecular basis for anti-amyloid therapy in the prevention and treatment of Alzheimer's disease. Neurobiol Aging. 2002;23(6):1009-1016.
58. Selkoe DJ. Amyloid β-protein and the genetics of Alzheimer's disease. J Biol Chem. 1996;271(31):18295-18298.
59. Landreth G. PPARgamma agonists as new therapeutic agents for the treatment of Alzheimer's disease. Exp Neurol. 2006;199(2):245-248.
60. Lagouge M, Argmann C, Gerhart-Hines Z, et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell. 2006;127(6):1109-1122.