Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease
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Spät, 2008, High- and low-calcium-dependent mechanisms of mitochondrial calcium signalling, Cell Calcium, 44, 51, 10.1016/j.ceca.2007.11.015
Hardy, 2006, A hundred years of Alzheimer's disease research, Neuron, 52, 3, 10.1016/j.neuron.2006.09.016
Murchison, 2007, Calcium buffering systems and calcium signaling in aged rat basal forebrain neurons, Aging Cell, 6, 297, 10.1111/j.1474-9726.2007.00293.x
Brown, 2004, Brain region-specific, age-related, alterations in mitochondrial responses to elevated calcium, J. Bioenerg. Biomembr., 36, 401, 10.1023/B:JOBB.0000041775.10388.23
Toescu, 2004, Ca2+ regulation and gene expression in normal brain aging, Trends Neurosci., 27, 614, 10.1016/j.tins.2004.07.010
Poon, 2006, Proteomics analysis provides insight into caloric restriction mediated oxidation and expression of brain proteins associated with age-related impaired cellular processes: mitochondrial dysfunction, glutamate dysregulation and impaired protein synthesis, Neurobiol. Aging, 27, 1020, 10.1016/j.neurobiolaging.2005.05.014
Blalock, 2003, Gene microarrays in hippocampal aging: statistical profiling identifies novel processes correlated with cognitive impairment, J. Neurosci., 23, 3807, 10.1523/JNEUROSCI.23-09-03807.2003
Emilsson, 2006, Alzheimer's disease: mRNA expression profiles of multiple patients show alterations of genes involved with calcium signaling, Neurobiol. Dis., 21, 618, 10.1016/j.nbd.2005.09.004
Mattson, 2004, Pathways towards and away from Alzheimer's disease, Nature, 430, 631, 10.1038/nature02621
Haass, 2007, Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide, Nat. Rev. Mol. Cell Biol., 8, 101, 10.1038/nrm2101
Mattson, 1992, β-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity, J. Neurosci., 12, 376, 10.1523/JNEUROSCI.12-02-00376.1992
Demuro, 2005, Calcium dysregulation and membrane disruption as a ubiquitous neurotoxic mechanism of soluble amyloid oligomers, J. Biol. Chem., 280, 17294, 10.1074/jbc.M500997200
Meyer-Luehmann, 2008, Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer's disease, Nature, 451, 720, 10.1038/nature06616
Furukawa, 1996, Activation of K+ channels and suppression of neuronal activity by secreted β-amyloid-precursor protein, Nature, 379, 74, 10.1038/379074a0
Leissring, 2002, A physiologic signaling role for the γ-secretase-derived intracellular fragment of APP, Proc. Natl. Acad. Sci. U. S. A., 99, 4697, 10.1073/pnas.072033799
Arispe, 1993, Alzheimer disease amyloid β protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum, Proc. Natl. Acad. Sci. U. S. A., 90, 567, 10.1073/pnas.90.2.567
Yoshiike, 2007, Pore-forming proteins share structural and functional homology with amyloid oligomers, Neuromolecular Med., 9, 270, 10.1007/s12017-007-0003-6
Lee, 2002, Annexin 5 and apolipoprotein E2 protect against Alzheimer's amyloid-β-peptide cytotoxicity by competitive inhibition at a common phosphatidylserine interaction site, Peptides, 23, 1249, 10.1016/S0196-9781(02)00060-8
Simakova, 2007, The cell-selective neurotoxicity of the Alzheimer's Aβ peptide is determined by surface phosphatidylserine and cytosolic ATP levels. Membrane binding is required for Aβ toxicity, J. Neurosci., 27, 13719, 10.1523/JNEUROSCI.3006-07.2007
Sahu, 2007, Phospholipid scramblases: an overview, Arch. Biochem. Biophys., 462, 103, 10.1016/j.abb.2007.04.002
Hensley, 1994, A model for β-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease, Proc. Natl. Acad. Sci. U. S. A., 91, 3270, 10.1073/pnas.91.8.3270
Huang, 1999, The A β peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction, Biochemistry, 38, 7609, 10.1021/bi990438f
Mark, 1997, Amyloid β-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation, J. Neurosci., 17, 1046, 10.1523/JNEUROSCI.17-03-01046.1997
Shankar, 2007, Natural oligomers of the Alzheimer amyloid-β protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway, J. Neurosci., 27, 2866, 10.1523/JNEUROSCI.4970-06.2007
Nimmrich, 2008, Amyloid β oligomers (A β (1-42) globulomer) suppress spontaneous synaptic activity by inhibition of P/Q-type calcium currents, J. Neurosci., 28, 788, 10.1523/JNEUROSCI.4771-07.2008
Liu, 2001, β-Amyloid peptide blocks the response of α 7-containing nicotinic receptors on hippocampal neurons, Proc. Natl. Acad. Sci. U. S. A., 98, 4734, 10.1073/pnas.081553598
Dougherty, 2003, β-Amyloid regulation of presynaptic nicotinic receptors in rat hippocampus and neocortex, J. Neurosci., 23, 6740, 10.1523/JNEUROSCI.23-17-06740.2003
Baker, 2000, Notch signaling in the nervous system. Pieces still missing from the puzzle, Bioessays, 22, 264, 10.1002/(SICI)1521-1878(200003)22:3<264::AID-BIES8>3.0.CO;2-M
Wang, 2004, Involvement of Notch signaling in hippocampal synaptic plasticity, Proc. Natl. Acad. Sci. U. S. A., 101, 9458, 10.1073/pnas.0308126101
Ito, 1994, Internal Ca2+ mobilization is altered in fibroblasts from patients with Alzheimer disease, Proc. Natl. Acad. Sci. U. S. A., 91, 534, 10.1073/pnas.91.2.534
Guo, 1996, Alzheimer's PS-1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid β-peptide, Neuroreport, 8, 379, 10.1097/00001756-199612200-00074
Guo, 1997, Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid β-peptide: involvement of calcium and oxyradicals, J. Neurosci., 17, 4212, 10.1523/JNEUROSCI.17-11-04212.1997
Leissring, 1999, Alzheimer's presenilin-1 mutation potentiates inositol 1,4,5-trisphosphate-mediated calcium signaling in Xenopus oocytes, J. Neurochem., 72, 1061, 10.1046/j.1471-4159.1999.0721061.x
Guo, 1999, Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice, Nat. Med., 5, 101, 10.1038/4789
Stutzmann, 2004, Dysregulated IP3 signaling in cortical neurons of knock-in mice expressing an Alzheimer's-linked mutation in presenilin1 results in exaggerated Ca2+ signals and altered membrane excitability, J. Neurosci., 24, 508, 10.1523/JNEUROSCI.4386-03.2004
Schneider, 2001, Mutant presenilins disturb neuronal calcium homeostasis in the brain of transgenic mice, decreasing the threshold for excitotoxicity and facilitating long-term potentiation, J. Biol. Chem., 276, 11539, 10.1074/jbc.M010977200
Begley, 1999, Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice, J. Neurochem., 72, 1030, 10.1046/j.1471-4159.1999.0721030.x
Chan, 2000, Presenilin-1 mutations increase levels of ryanodine receptors and calcium release in PC12 cells and cortical neurons, J. Biol. Chem., 275, 18195, 10.1074/jbc.M000040200
Pack-Chung, 2000, Presenilin 2 interacts with sorcin, a modulator of the ryanodine receptor, J. Biol. Chem., 275, 14440, 10.1074/jbc.M909882199
Stabler, 1999, A myristoylated calcium-binding protein that preferentially interacts with the Alzheimer's disease presenilin 2 protein, J. Cell Biol., 145, 1277, 10.1083/jcb.145.6.1277
Buxbaum, 1998, Calsenilin: a calcium-binding protein that interacts with the presenilins and regulates the levels of a presenilin fragment, Nat. Med., 4, 1177, 10.1038/2673
Green, 2008, SERCA pump activity is physiologically regulated by presenilin and regulates amyloid β production, J. Cell Biol., 181, 1107, 10.1083/jcb.200706171
Cai, 2006, The presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosis, J. Biol. Chem., 281, 16649, 10.1074/jbc.M512026200
Cheung, 2008, Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating, Neuron, 58, 871, 10.1016/j.neuron.2008.04.015
Stutzmann, 2006, Enhanced ryanodine receptor recruitment contributes to Ca2+ disruptions in young, adult, and aged Alzheimer's disease mice, J. Neurosci., 26, 5180, 10.1523/JNEUROSCI.0739-06.2006
Tu, 2006, Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations, Cell, 126, 981, 10.1016/j.cell.2006.06.059
Nelson, 2007, Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1, J. Clin. Invest., 117, 1230, 10.1172/JCI30447
Cedazo-Minguez, 2002, The presenilin 1 δE9 mutation gives enhanced basal phospholipase C activity and a resultant increase in intracellular calcium concentrations, J. Biol. Chem., 277, 36646, 10.1074/jbc.M112117200
Dumanchin, 2006, Biological effects of four PSEN1 gene mutations causing Alzheimer disease with spastic paraparesis and cotton wool plaques, Hum. Mutat., 27, 1063, 10.1002/humu.9458
McKee, 1990, Hippocampal neurons predisposed to neurofibrillary tangle formation are enriched in type II calcium/calmodulin-dependent protein kinase, J. Neuropathol. Exp. Neurol., 49, 49, 10.1097/00005072-199001000-00006
Nixon, 2003, The calpains in aging and aging-related diseases, Ageing Res. Rev., 2, 407, 10.1016/S1568-1637(03)00029-1
Botella-Lopez, 2006, Reelin expression and glycosylation patterns are altered in Alzheimer's disease, Proc. Natl. Acad. Sci. U. S. A., 103, 5573, 10.1073/pnas.0601279103
Mattson, 1990, Antigenic changes similar to those seen in neurofibrillary tangles are elicited by glutamate and Ca2+ influx in cultured hippocampal neurons, Neuron, 4, 105, 10.1016/0896-6273(90)90447-N
Furukawa, 2003, Alteration in calcium channel properties is responsible for the neurotoxic action of a familial frontotemporal dementia tau mutation, J. Neurochem., 87, 427, 10.1046/j.1471-4159.2003.02020.x
Querfurth, 1994, Calcium ionophore increases amyloid β peptide production by cultured cells, Biochemistry, 33, 4550, 10.1021/bi00181a016
Zhang, 2007, Hypoxia-inducible factor 1α (HIF-1α)-mediated hypoxia increases BACE1 expression and β-amyloid generation, J. Biol. Chem., 282, 10873, 10.1074/jbc.M608856200
Buxbaum, 1994, Calcium regulates processing of the Alzheimer amyloid protein precursor in a protein kinase C-independent manner, Proc. Natl. Acad. Sci. U. S. A., 91, 4489, 10.1073/pnas.91.10.4489
Petryniak, 1996, Elevated intracellular calcium concentration increases secretory processing of the amyloid precursor protein by a tyrosine phosphorylation-dependent mechanism, Biochem. J., 320, 957, 10.1042/bj3200957
Lazarov, 2002, Evidence that synaptically released β-amyloid accumulates as extracellular deposits in the hippocampus of transgenic mice, J. Neurosci., 22, 9785, 10.1523/JNEUROSCI.22-22-09785.2002
Spires-Jones, 2007, Impaired spine stability underlies plaque-related spine loss in an Alzheimer's disease mouse model, Am. J. Pathol., 171, 1304, 10.2353/ajpath.2007.070055
Celsi, 2007, β-Amyloid causes downregulation of calcineurin in neurons through induction of oxidative stress, Neurobiol. Dis., 26, 342, 10.1016/j.nbd.2006.12.022
Lacor, 2007, 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, 10.1523/JNEUROSCI.3501-06.2007
Janus, 2000, A β peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease, Nature, 408, 979, 10.1038/35050110
Palop, 2007, Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease, Neuron, 55, 697, 10.1016/j.neuron.2007.07.025
Priller, 2007, Mutant presenilin 1 alters synaptic transmission in cultured hippocampal neurons, J. Biol. Chem., 282, 1119, 10.1074/jbc.M605066200
Shemer, 2006, Non-fibrillar β-amyloid abates spike-timing-dependent synaptic potentiation at excitatory synapses in layer 2/3 of the neocortex by targeting postsynaptic AMPA receptors, Eur. J. Neurosci., 23, 2035, 10.1111/j.1460-9568.2006.04733.x
Haughey, 2002, Disruption of neurogenesis by amyloid β-peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease, J. Neurochem., 83, 1509, 10.1046/j.1471-4159.2002.01267.x
Huang, 2006, Apolipoprotein E and Alzheimer disease, Neurology, 66, S79, 10.1212/01.wnl.0000192102.41141.9e
Hartmann, 1994, Apolipoprotein E and cholesterol affect neuronal calcium signalling: the possible relationship to β-amyloid neurotoxicity, Biochem. Biophys. Res. Commun., 200, 1185, 10.1006/bbrc.1994.1576
Chen, 2005, Reelin modulates NMDA receptor activity in cortical neurons, J. Neurosci., 25, 8209, 10.1523/JNEUROSCI.1951-05.2005
Chin, 2007, Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease, J. Neurosci., 27, 2727, 10.1523/JNEUROSCI.3758-06.2007
Iritani, 2001, Relationship of calbindin D28K-immunoreactive cells and neuropathological changes in the hippocampal formation of Alzheimer's disease, Neuropathology, 21, 162, 10.1046/j.1440-1789.2001.00393.x
Geula, 2003, Loss of calbindin-D28k from aging human cholinergic basal forebrain: relation to neuronal loss, J. Comp. Neurol., 455, 249, 10.1002/cne.10475
Mikkonen, 1999, Subfield- and layer-specific changes in parvalbumin, calretinin and calbindin-D28K immunoreactivity in the entorhinal cortex in Alzheimer's disease, Neuroscience, 92, 515, 10.1016/S0306-4522(99)00047-0
Mishizen-Eberz, 2004, Biochemical and molecular studies of NMDA receptor subunits NR1/2A/2B in hippocampal subregions throughout progression of Alzheimer's disease pathology, Neurobiol. Dis., 15, 80, 10.1016/j.nbd.2003.09.016
Lazarov, 2005, Environmental enrichment reduces Aβ levels and amyloid deposition in transgenic mice, Cell, 120, 701, 10.1016/j.cell.2005.01.015
Wolf, 2006, Cognitive and physical activity differently modulate disease progression in the amyloid precursor protein (APP)-23 model of Alzheimer's disease, Biol. Psychiatry, 60, 1314, 10.1016/j.biopsych.2006.04.004
Halagappa, 2007, Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer's disease, Neurobiol. Dis., 26, 212, 10.1016/j.nbd.2006.12.019
Mattson, 2004, BDNF and 5-HT: a dynamic duo in age-related neuronal plasticity and neurodegenerative disorders, Trends Neurosci., 27, 589, 10.1016/j.tins.2004.08.001
Schmidt, 2006, Inhibitors and modulators of β- and γ-secretase, Curr. Top. Med. Chem., 6, 377, 10.2174/156802606776287027
Lipton, 2006, Paradigm shift in neuroprotection by NMDA receptor blockade: memantine and beyond, Nat. Rev. Drug Discov., 5, 160, 10.1038/nrd1958
Bachurin, 2001, Antihistamine agent Dimebon as a novel neuroprotector and a cognition enhancer, Ann. N. Y. Acad. Sci., 939, 425, 10.1111/j.1749-6632.2001.tb03654.x
Grigorev, 2003, Comparative study of action mechanisms of dimebon and memantine on AMPA- and NMDA-subtypes glutamate receptors in rat cerebral neurons, Bull. Exp. Biol. Med., 136, 474, 10.1023/B:BEBM.0000017097.75818.14
Lindholm, 2006, ER stress and neurodegenerative diseases, Cell Death Differ., 13, 385, 10.1038/sj.cdd.4401778
Chan, 2004, Herp stabilizes neuronal Ca2+ homeostasis and mitochondrial function during endoplasmic reticulum stress, J. Biol. Chem., 279, 28733, 10.1074/jbc.M404272200
Thiffault, 2005, Cyclical mitochondrial δψM fluctuations linked to electron transport, F0F1 ATP-synthase and mitochondrial Na+/Ca+2 exchange are reduced in Alzheimer's disease cybrids, Mitochondrion, 5, 109, 10.1016/j.mito.2004.12.002