Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase

Nature Medicine - Tập 14 Số 7 - Trang 723-730 - 2008
Mohammad Ali Faghihi1,2, Farzaneh Modarresi3, Ahmad M. Khalil3, Douglas E. Wood4, Barbara G. Sahagan4, Todd E. Morgan5, Caleb E. Finch5, Georges St. Laurent6,7, Paul J. Kenny3, Claes Wahlestedt3
1Department of Molecular Medicine and Surgery, Karolinska Institute, Solna (L1:00), Stockholm, Sweden
2Molecular and Integrative Neurosciences Department, The Scripps Research Institute, Jupiter, USA
3Scripps Research Institute#TAB#
4Pfizer
5University of Southern California
6Department of Biochemistry and Molecular Biology, The George Washington University Medical Center, Washington, USA
7Immunovirology—Biogenesis Group, University of Antioquia, Medellín, Colombia

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Goedert, M. & Spillantini, M.G. A century of Alzheimer's disease. Science 314, 777–781 (2006).

Faghihi, M.A., Mottagui-Tabar, S. & Wahlestedt, C. Genetics of neurological disorders. Expert Rev. Mol. Diagn. 4, 317–332 (2004).

Monaco, S., Zanusso, G., Mazzucco, S. & Rizzuto, N. Cerebral amyloidoses: molecular pathways and therapeutic challenges. Curr. Med. Chem. 13, 1903–1913 (2006).

Lacor, P.N. et al. Aβ oligomer–induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease. J. Neurosci. 27, 796–807 (2007).

Zhu, D. et al. Phospholipases A2 mediate amyloid-β peptide–induced mitochondrial dysfunction. J. Neurosci. 26, 11111–11119 (2006).

Esposito, G. et al. CB1 receptor selective activation inhibits β-amyloid–induced iNOS protein expression in C6 cells and subsequently blunts tau protein hyperphosphorylation in co-cultured neurons. Neurosci. Lett. 404, 342–346 (2006).

Snyder, E.M. et al. Regulation of NMDA receptor trafficking by amyloid-β. Nat. Neurosci. 8, 1051–1058 (2005).

Matsuyama, S., Teraoka, R., Mori, H. & Tomiyama, T. Inverse correlation between amyloid precursor protein and synaptic plasticity in transgenic mice. Neuroreport 18, 1083–1087 (2007).

Abramov, A.Y., Canevari, L. & Duchen, M.R. β-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase. J. Neurosci. 24, 565–575 (2004).

Ohyagi, Y. et al. Intracellular Aβ42 activates p53 promoter: a pathway to neurodegeneration in Alzheimer's disease. FASEB J. 19, 255–257 (2005).

Zhao, J. et al. β-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis. J. Neurosci. 27, 3639–3649 (2007).

Sun, X. et al. Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression. Proc. Natl. Acad. Sci. USA 103, 18727–18732 (2006).

Tong, Y. et al. Oxidative stress potentiates BACE1 gene expression and Aβ generation. J. Neural Transm. 112, 455–469 (2005).

Li, R. et al. Amyloid β peptide load is correlated with increased β-secretase activity in sporadic Alzheimer's disease patients. Proc. Natl. Acad. Sci. USA 101, 3632–3637 (2004).

Holsinger, R.M., McLean, C.A., Collins, S.J., Masters, C.L. & Evin, G. Increased β-secretase activity in cerebrospinal fluid of Alzheimer's disease subjects. Ann. Neurol. 55, 898–899 (2004).

Fukumoto, H., Cheung, B.S., Hyman, B.T. & Irizarry, M.C. β-secretase protein and activity are increased in the neocortex in Alzheimer disease. Arch. Neurol. 59, 1381–1389 (2002).

Johnston, J.A. et al. Expression and activity of β-site amyloid precursor protein cleaving enzyme in Alzheimer's disease. Biochem. Soc. Trans. 33, 1096–1100 (2005).

Ohno, M. et al. BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer's disease. Neuron 41, 27–33 (2004).

Tesco, G. et al. Depletion of GGA3 stabilizes BACE and enhances β-secretase activity. Neuron 54, 721–737 (2007).

Ma, H. et al. Involvement of β-site APP cleaving enzyme 1 (BACE1) in amyloid precursor protein–mediated enhancement of memory and activity-dependent synaptic plasticity. Proc. Natl. Acad. Sci. USA 104, 8167–8172 (2007).

Laird, F.M. et al. BACE1, a major determinant of selective vulnerability of the brain to amyloid-β amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J. Neurosci. 25, 11693–11709 (2005).

Hu, X. et al. Bace1 modulates myelination in the central and peripheral nervous system. Nat. Neurosci. 9, 1520–1525 (2006).

Willem, M. et al. Control of peripheral nerve myelination by the β-secretase BACE1. Science 314, 664–666 (2006).

Engstrom, P.G. et al. Complex loci in human and mouse genomes. PLoS Genet. 2, e47 (2006).

Katayama, S. et al. Antisense transcription in the mammalian transcriptome. Science 309, 1564–1566 (2005).

Wahlestedt, C. Natural antisense and noncoding RNA transcripts as potential drug targets. Drug Discov. Today 11, 503–508 (2006).

Su, Y., Ryder, J. & Ni, B. Inhibition of Aβ production and APP maturation by a specific PKA inhibitor. FEBS Lett. 546, 407–410 (2003).

Thakker, D.R., Hoyer, D. & Cryan, J.F. Interfering with the brain: use of RNA interference for understanding the pathophysiology of psychiatric and neurological disorders. Pharmacol. Ther. 109, 413–438 (2006).

Borghi, R. et al. The increased activity of BACE1 correlates with oxidative stress in Alzheimer's disease. Neurobiol. Aging 28, 1009–1014 (2006).

Tamagno, E., Bardini, P., Guglielmotto, M., Danni, O. & Tabaton, M. The various aggregation states of β-amyloid 1–42 mediate different effects on oxidative stress, neurodegeneration, and BACE-1 expression. Free Radic. Biol. Med. 41, 202–212 (2006).

Harkany, T. et al. Mechanisms of β-amyloid neurotoxicity: perspectives of pharmacotherapy. Rev. Neurosci. 11, 329–382 (2000).

Yatin, S.M. et al. Temporal relations among amyloid β-peptide–induced free-radical oxidative stress, neuronal toxicity, and neuronal defensive responses. J. Mol. Neurosci. 11, 183–197 (1998).

Meyer-Luehmann, M. et al. Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer's disease. Nature 451, 720–724 (2008).

Walsh, D.M. et al. The role of cell-derived oligomers of Aβ in Alzheimer's disease and avenues for therapeutic intervention. Biochem. Soc. Trans. 33, 1087–1090 (2005).

Link, C.D. et al. Gene expression analysis in a transgenic Caenorhabditis elegans Alzheimer's disease model. Neurobiol. Aging 24, 397–413 (2003).

Ray, S. et al. Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins. Nat. Med. 13, 1359–1362 (2007).

Chishti, M.A. et al. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. J. Biol. Chem. 276, 21562–21570 (2001).

Li, F. et al. Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice. J. Neurochem. 89, 1308–1312 (2004).

McConlogue, L. et al. Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP transgenic mice. J. Biol. Chem. 282, 26326–26334 (2007).

Zhong, Z. et al. Levels of β-secretase (BACE1) in cerebrospinal fluid as a predictor of risk in mild cognitive impairment. Arch. Gen. Psychiatry 64, 718–726 (2007).

Li, Y., Zhou, W., Tong, Y., He, G. & Song, W. Control of APP processing and Aβ generation level by BACE1 enzymatic activity and transcription. FASEB J. 20, 285–292 (2006).

Cirrito, J.R. et al. Synaptic activity regulates interstitial fluid amyloid-β levels in vivo. Neuron 48, 913–922 (2005).

Emilsson, L., Saetre, P. & Jazin, E. Alzheimer's disease: mRNA expression profiles of multiple patients show alterations of genes involved with calcium signaling. Neurobiol. Dis. 21, 618–625 (2006).

Brooks, W.M. et al. Gene expression profiles of metabolic enzyme transcripts in Alzheimer's disease. Brain Res. 1127, 127–135 (2007).

Rossner, S., Sastre, M., Bourne, K. & Lichtenthaler, S.F. Transcriptional and translational regulation of BACE1 expression–implications for Alzheimer's disease. Prog. Neurobiol. 79, 95–111 (2006).

Holsinger, R.M., McLean, C.A., Beyreuther, K., Masters, C.L. & Evin, G. Increased expression of the amyloid precursor β-secretase in Alzheimer's disease. Ann. Neurol. 51, 783–786 (2002).

Hsieh, H. et al. AMPAR removal underlies Aβ-induced synaptic depression and dendritic spine loss. Neuron 52, 831–843 (2006).

St Laurent, G., III & Wahlestedt, C. Noncoding RNAs: couplers of analog and digital information in nervous system function? Trends Neurosci. 30, 612–621 (2007).

Vassar, R. The β-secretase, BACE: a prime drug target for Alzheimer's disease. J. Mol. Neurosci. 17, 157–170 (2001).

Kumar, P. et al. Transvascular delivery of small interfering RNA to the central nervous system. Nature 448, 39–43 (2007).