Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase (original) (raw)
Goedert, M. & Spillantini, M.G. A century of Alzheimer's disease. Science314, 777–781 (2006). ArticleCAS Google Scholar
Faghihi, M.A., Mottagui-Tabar, S. & Wahlestedt, C. Genetics of neurological disorders. Expert Rev. Mol. Diagn.4, 317–332 (2004). ArticleCAS Google Scholar
Monaco, S., Zanusso, G., Mazzucco, S. & Rizzuto, N. Cerebral amyloidoses: molecular pathways and therapeutic challenges. Curr. Med. Chem.13, 1903–1913 (2006). Article Google Scholar
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). ArticleCAS Google Scholar
Zhu, D. et al. Phospholipases A2 mediate amyloid-β peptide–induced mitochondrial dysfunction. J. Neurosci.26, 11111–11119 (2006). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Snyder, E.M. et al. Regulation of NMDA receptor trafficking by amyloid-β. Nat. Neurosci.8, 1051–1058 (2005). ArticleCAS Google Scholar
Matsuyama, S., Teraoka, R., Mori, H. & Tomiyama, T. Inverse correlation between amyloid precursor protein and synaptic plasticity in transgenic mice. Neuroreport18, 1083–1087 (2007). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Ohyagi, Y. et al. Intracellular Aβ42 activates p53 promoter: a pathway to neurodegeneration in Alzheimer's disease. FASEB J.19, 255–257 (2005). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Sun, X. et al. Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression. Proc. Natl. Acad. Sci. USA103, 18727–18732 (2006). ArticleCAS Google Scholar
Tong, Y. et al. Oxidative stress potentiates BACE1 gene expression and Aβ generation. J. Neural Transm.112, 455–469 (2005). ArticleCAS Google Scholar
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. USA101, 3632–3637 (2004). ArticleCAS Google Scholar
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). Article Google Scholar
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). Article Google Scholar
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). ArticleCAS Google Scholar
Ohno, M. et al. BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer's disease. Neuron41, 27–33 (2004). ArticleCAS Google Scholar
Tesco, G. et al. Depletion of GGA3 stabilizes BACE and enhances β-secretase activity. Neuron54, 721–737 (2007). ArticleCAS Google Scholar
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. USA104, 8167–8172 (2007). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Hu, X. et al. Bace1 modulates myelination in the central and peripheral nervous system. Nat. Neurosci.9, 1520–1525 (2006). ArticleCAS Google Scholar
Willem, M. et al. Control of peripheral nerve myelination by the β-secretase BACE1. Science314, 664–666 (2006). ArticleCAS Google Scholar
Engstrom, P.G. et al. Complex loci in human and mouse genomes. PLoS Genet.2, e47 (2006). Article Google Scholar
Katayama, S. et al. Antisense transcription in the mammalian transcriptome. Science309, 1564–1566 (2005). Article Google Scholar
Wahlestedt, C. Natural antisense and noncoding RNA transcripts as potential drug targets. Drug Discov. Today11, 503–508 (2006). ArticleCAS Google Scholar
Su, Y., Ryder, J. & Ni, B. Inhibition of Aβ production and APP maturation by a specific PKA inhibitor. FEBS Lett.546, 407–410 (2003). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Borghi, R. et al. The increased activity of BACE1 correlates with oxidative stress in Alzheimer's disease. Neurobiol. Aging28, 1009–1014 (2006). Article Google Scholar
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). ArticleCAS Google Scholar
Harkany, T. et al. Mechanisms of β-amyloid neurotoxicity: perspectives of pharmacotherapy. Rev. Neurosci.11, 329–382 (2000). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Meyer-Luehmann, M. et al. Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer's disease. Nature451, 720–724 (2008). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Link, C.D. et al. Gene expression analysis in a transgenic Caenorhabditis elegans Alzheimer's disease model. Neurobiol. Aging24, 397–413 (2003). ArticleCAS Google Scholar
Ray, S. et al. Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins. Nat. Med.13, 1359–1362 (2007). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Li, F. et al. Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice. J. Neurochem.89, 1308–1312 (2004). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Zhong, Z. et al. Levels of β-secretase (BACE1) in cerebrospinal fluid as a predictor of risk in mild cognitive impairment. Arch. Gen. Psychiatry64, 718–726 (2007). ArticleCAS Google Scholar
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). Article Google Scholar
Cirrito, J.R. et al. Synaptic activity regulates interstitial fluid amyloid-β levels in vivo. Neuron48, 913–922 (2005). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Brooks, W.M. et al. Gene expression profiles of metabolic enzyme transcripts in Alzheimer's disease. Brain Res.1127, 127–135 (2007). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
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). ArticleCAS Google Scholar
Hsieh, H. et al. AMPAR removal underlies Aβ-induced synaptic depression and dendritic spine loss. Neuron52, 831–843 (2006). ArticleCAS Google Scholar
St Laurent, G., III & Wahlestedt, C. Noncoding RNAs: couplers of analog and digital information in nervous system function? Trends Neurosci.30, 612–621 (2007). ArticleCAS Google Scholar
Vassar, R. The β-secretase, BACE: a prime drug target for Alzheimer's disease. J. Mol. Neurosci.17, 157–170 (2001). ArticleCAS Google Scholar
Kumar, P. et al. Transvascular delivery of small interfering RNA to the central nervous system. Nature448, 39–43 (2007). ArticleCAS Google Scholar