SEARCH

SEARCH BY CITATION

References

  • 1
    Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA & Katzman R (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30, 572580.
  • 2
    DeKosky S & Scheff S (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27, 457464.
  • 3
    DeKosky ST, Scheff SW & Styren SD (1996) Structural correlates of cognition in dementia: quantification and assessment of synapse change. Neurodegeneration 5, 417421.
  • 4
    Sisodia SS & Price DL (1995) Role of the beta-amyloid protein in Alzheimer’s disease. FASEB J 9, 366370.
  • 5
    Selkoe D (1989) Amyloid β protein precursor and the pathogenesis of Alzheimer’s disease. Cell 58, 611612.
  • 6
    Selkoe D (1990) Amyloid β-protein deposition as a seminal pathogenic event in AD: an hypothesis. Neurobiol Aging 11, 299.
  • 7
    Selkoe D (1993) Physiological production of the β-amyloid protein and the mechanisms of Alzheimer’s disease. Trends Neurosci 16, 403409.
  • 8
    Klein WL (2002) Abeta toxicity in Alzheimer’s disease: globular oligomers (ADDLs) as new vaccine and drug targets. Neurochem Int 41, 345352.
  • 9
    Klein WL, Krafft GA & Finch CE (2001) Targeting small Abeta oligomers: the solution to an Alzheimer’s disease conundrum? Trends Neurosci 24, 219224.
  • 10
    Walsh DM & Selkoe DJ (2004) Oligomers on the brain: the emerging role of soluble protein aggregates in neurodegeneration. Protein Pept Lett 11, 213228.
  • 11
    Glabe CC (2005) Amyloid accumulation and pathogenesis of Alzheimer’s disease: significance of monomeric, oligomeric and fibrillar Abeta. Subcell Biochem 38, 167177.
  • 12
    Lambert MP, Barlow AK, Chromy BA, Edwards C, Freed R, Liosatos M, Morgan TE, Rozovsky I, Trommer B, Viola KL et al. (1998) Diffusible, nonfibrillar ligands derived from Abeta1–42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 95, 64486453.
  • 13
    Selkoe DJ (2008) Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. Behav Brain Res 192, 106113.
  • 14
    Caughey B & Lansbury PT (2003) Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. Annu Rev Neurosci 26, 267298.
  • 15
    Teplow DB (1998) Structural and kinetic features of amyloid beta-protein fibrillogenesis. Amyloid 5, 121142.
  • 16
    Walsh DM, Klyubin I, Fadeeva JV, Cullen WK, Anwyl R, Wolfe MS, Rowan MJ & Selkoe DJ (2002) Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416, 535539.
  • 17
    Lesne S, Koh MT, Kotilinek L, Kayed R, Glabe CG, Yang A, Gallagher M & Ashe KH (2006) A specific amyloid-beta protein assembly in the brain impairs memory. Nature 440, 352357.
  • 18
    Townsend M, Shankar GM, Mehta T, Walsh DM & Selkoe DJ (2006) Effects of secreted oligomers of amyloid beta-protein on hippocampal synaptic plasticity: a potent role for trimers. J Physiol 572, 477492.
  • 19
    Klyubin I, Betts V, Welzel AT, Blennow K, Zetterberg H, Wallin A, Lemere CA, Cullen WK, Peng Y, Wisniewski T et al. (2008) Amyloid beta protein dimer-containing human CSF disrupts synaptic plasticity: prevention by systemic passive immunization. J Neurosci 28, 42314237.
  • 20
    Lacor PN, Buniel MC, Furlow PW, Clemente AS, Velasco PT, Wood M, Viola KL & Klein WL (2007) Abeta oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer’s disease. J Neurosci 27, 796807.
  • 21
    Gylys KH, Fein JA, Yang F, Wiley DJ, Miller CA & Cole GM (2004) Synaptic changes in Alzheimer’s disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence. Am J Pathol 165, 18091817.
  • 22
    Koffie RM, Meyer-Luehmann M, Hashimoto T, Adams KW, Mielke ML, Garcia-Alloza M, Micheva KD, Smith SJ, Kim ML, Lee VM et al. (2009) Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques. Proc Natl Acad Sci USA 106, 40124017.
  • 23
    Simon AM, Schiapparelli L, Salazar-Colocho P, Cuadrado-Tejedor M, Escribano L, Lopez de Maturana R, Del Rio J, Perez-Mediavilla A & Frechilla D (2009) Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Abeta levels. Neurobiol Dis 33, 369378.
  • 24
    Sultana R, Banks WA & Butterfield DA (2010) Decreased levels of PSD95 and two associated proteins and increased levels of BCl2 and caspase 3 in hippocampus from subjects with amnestic mild cognitive impairment: insights into their potential roles for loss of synapses and memory, accumulation of Abeta, and neurodegeneration in a prodromal stage of Alzheimer’s disease. J Neurosci Res 88, 469477.
  • 25
    Almeida CG, Tampellini D, Takahashi RH, Greengard P, Lin MT, Snyder EM & Gouras GK (2005) Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses. Neurobiol Dis 20, 187198.
  • 26
    Masliah E, Rockenstein E, Veinbergs I, Mallory M, Hashimoto M, Takeda A, Sagara Y, Sisk A & Mucke L (2000) Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. Science 287, 12651269.
  • 27
    Cole G, Dobkins K, Hansen L, Terry R & Saitoh T (1988) Decreased levels of protein kinase C in Alzheimer brain. Brain Res 452, 165170.
  • 28
    Segal M (2005) Dendritic spines and long-term plasticity. Nat Rev Neurosci 6, 277284.
  • 29
    Shrestha BR, Vitolo OV, Joshi P, Lordkipanidze T, Shelanski M & Dunaevsky A (2006) Amyloid beta peptide adversely affects spine number and motility in hippocampal neurons. Mol Cell Neurosci 33, 274282.
  • 30
    Naisbitt S, Kim E, Tu JC, Xiao B, Sala C, Valtschanoff J, Weinberg RJ, Worley PF & Sheng M (1999) Shank, a novel family of postsynaptic density proteins that binds to the NMDA receptor/PSD-95/GKAP complex and cortactin. Neuron 23, 569582.
  • 31
    Boeckers TM, Bockmann J, Kreutz MR & Gundelfinger ED (2002) ProSAP/Shank proteins – a family of higher order organizing molecules of the postsynaptic density with an emerging role in human neurological disease. J Neurochem 81, 903910.
  • 32
    Qualmann B, Boeckers TM, Jeromin M, Gundelfinger ED & Kessels MM (2004) Linkage of the actin cytoskeleton to the postsynaptic density via direct interactions of Abp1 with the ProSAP/Shank family. J Neurosci 24, 24812495.
  • 33
    Viola KL, Velasco PT & Klein WL (2008) Why Alzheimer’s is a disease of memory: the attack on synapses by A beta oligomers (ADDLs). J Nutr Health Aging 12, 51S57S.
  • 34
    Lacor PN, Buniel MC, Chang L, Fernandez SJ, Gong Y, Viola KL, Lambert MP, Velasco PT, Bigio EH, Finch CE et al. (2004) Synaptic targeting by Alzheimer’s-related amyloid beta oligomers. J Neurosci 24, 1019110200.
  • 35
    Moreno H, Yu E, Pigino G, Hernandez AI, Kim N, Moreira JE, Sugimori M & Llinas RR (2009) Synaptic transmission block by presynaptic injection of oligomeric amyloid beta. Proc Natl Acad Sci USA 106, 59015906.
  • 36
    Shankar GM, Bloodgood BL, Townsend M, Walsh DM, Selkoe DJ & Sabatini BL (2007) Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway. J Neurosci 27, 28662875.
  • 37
    Shankar GM, Li S, Mehta TH, Garcia-Munoz A, Shepardson NE, Smith I, Brett FM, Farrell MA, Rowan MJ, Lemere CA et al. (2008) Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic plasticity and memory. Nat Med 14, 837842.
  • 38
    Roselli F, Tirard M, Lu J, Hutzler P, Lamberti P, Livrea P, Morabito M & Almeida OF (2005) Soluble beta-amyloid1–40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses. J Neurosci 25, 1106111070.
  • 39
    Roselli F, Hutzler P, Wegerich Y, Livrea P & Almeida OF (2009) Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1–40) through divergent NMDAR-dependent signalling pathways. PLoS ONE 4, e6011.
  • 40
    Kayed R, Head E, Thompson JL, McIntire TM, Milton SC, Cotman CW & Glabe CG (2003) Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis. Science 300, 486489.
  • 41
    Gong Y, Chang L, Viola KL, Lacor PN, Lambert MP, Finch CE, Krafft GA & Klein WL (2003) Alzheimer’s disease-affected brain: presence of oligomeric A beta ligands (ADDLs) suggests a molecular basis for reversible memory loss. Proc Natl Acad Sci USA 100, 1041710422.
  • 42
    Chafekar SM, Baas F & Scheper W (2008) Oligomer-specific Abeta toxicity in cell models is mediated by selective uptake. Biochim Biophys Acta 1782, 523531.
  • 43
    Yang AJ, Chandswangbhuvana D, Margol L & Glabe CG (1998) Loss of endosomal/lysosomal membrane impermeability is an early event in amyloid Abeta1–42 pathogenesis. J Neurosci Res 52, 691698.
  • 44
    Glabe C (2001) Intracellular mechanisms of amyloid accumulation and pathogenesis in Alzheimer’s disease. J Mol Neurosci 17, 137145.
  • 45
    Cho KO, Hunt CA & Kennedy MB (1992) The rat brain postsynaptic density fraction contains a homolog of the Drosophila discs-large tumor suppressor protein. Neuron 9, 929942.
  • 46
    Kornau HC, Schenker LT, Kennedy MB & Seeburg PH (1995) Domain interaction between NMDA receptor subunits and the postsynaptic density protein PSD-95. Science 269, 17371740.
  • 47
    Niethammer M, Kim E & Sheng M (1996) Interaction between the C terminus of NMDA receptor subunits and multiple members of the PSD-95 family of membrane-associated guanylate kinases. J Neurosci 16, 21572163.
  • 48
    Kistner U, Wenzel BM, Veh RW, Cases-Langhoff C, Garner AM, Appeltauer U, Voss B, Gundelfinger ED & Garner CC (1993) SAP90, a rat presynaptic protein related to the product of the Drosophila tumor suppressor gene dlg-A. J Biol Chem 268, 45804583.
  • 49
    Sprengel R, Suchanek B, Amico C, Brusa R, Burnashev N, Rozov A, Hvalby O, Jensen V, Paulsen O, Andersen P et al. (1998) Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo. Cell 92, 279289.
  • 50
    Migaud M, Charlesworth P, Dempster M, Webster LC, Watabe AM, Makhinson M, He Y, Ramsay MF, Morris RG, Morrison JH et al. (1998) Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein. Nature 396, 433439.
  • 51
    Sheng M & Kim E (2000) The Shank family of scaffold proteins. J Cell Sci 113 (Pt 11), 18511856.
  • 52
    Ehlers MD (2002) Molecular morphogens for dendritic spines. Trends Neurosci 25, 6467.
  • 53
    Kim E, Naisbitt S, Hsueh YP, Rao A, Rothschild A, Craig AM & Sheng M (1997) GKAP, a novel synaptic protein that interacts with the guanylate kinase-like domain of the PSD-95/SAP90 family of channel clustering molecules. J Cell Biol 136, 669678.
  • 54
    Tu JC, Xiao B, Naisbitt S, Yuan JP, Petralia RS, Brakeman P, Doan A, Aakalu VK, Lanahan AA, Sheng M et al. (1999) Coupling of mGluR/Homer and PSD-95 complexes by the Shank family of postsynaptic density proteins. Neuron 23, 583592.
  • 55
    Xiao B, Tu JC, Petralia RS, Yuan JP, Doan A, Breder CD, Ruggiero A, Lanahan AA, Wenthold RJ & Worley PF (1998) Homer regulates the association of group 1 metabotropic glutamate receptors with multivalent complexes of homer-related, synaptic proteins. Neuron 21, 707716.
  • 56
    Boeckers TM, Kreutz MR, Winter C, Zuschratter W, Smalla KH, Sanmarti-Vila L, Wex H, Langnaese K, Bockmann J, Garner CC et al. (2001) Proline-rich synapse-associated protein-1/cortactin binding protein 1 (ProSAP1/CortBP1) is a PDZ-domain protein highly enriched in the postsynaptic density. Ann Anat 183, 101.
  • 57
    Gong Y, Lippa CF, Zhu J, Lin Q & Rosso AL (2009) Disruption of glutamate receptors at Shank-postsynaptic platform in Alzheimer’s disease. Brain Res 1292, 191198.
  • 58
    Bonaglia MC, Giorda R, Borgatti R, Felisari G, Gagliardi C, Selicorni A & Zuffardi O (2001) Disruption of the ProSAP2 gene in a t(12;22)(q24.1;q13.3) is associated with the 22q13.3 deletion syndrome. Am J Hum Genet 69, 261268.
  • 59
    Wilson HL, Wong AC, Shaw SR, Tse WY, Stapleton GA, Phelan MC, Hu S, Marshall J & McDermid HE (2003) Molecular characterisation of the 22q13 deletion syndrome supports the role of haploinsufficiency of SHANK3/PROSAP2 in the major neurological symptoms. J Med Genet 40, 575584.
  • 60
    Hsieh H, Boehm J, Sato C, Iwatsubo T, Tomita T, Sisodia S & Malinow R (2006) AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss. Neuron 52, 831843.
  • 61
    Rockenstein E, Mallory M, Mante M, Sisk A & Masliah E (2001) Early formation of mature amyloid-b protein deposits in a mutant APP transgenic model depends on levels of Ab1–42. J Neurosci Res 66, 573582.
  • 62
    Rockenstein E, Mallory M, Mante M, Alford M, Windisch M, Moessler H & Masliah E (2002) Effects of cerebrolysin on amyloid-beta deposition in a transgenic model of Alzheimer’s disease. J Neural Transm Suppl, 62, 327336.
  • 63
    Marongiu R, Spencer B, Crews L, Adame A, Patrick C, Trejo M, Dallapiccola B, Valente EM & Masliah E (2009) Mutant Pink1 induces mitochondrial dysfunction in a neuronal cell model of Parkinson’s disease by disturbing calcium flux. J Neurochem 108, 15611574.
  • 64
    Hashimoto M, Rockenstein E, Mante M, Mallory M & Masliah E (2001) β-Synuclein inhibits alpha-synuclein aggregation: a possible role as an anti-parkinsonian factor. Neuron 32, 213223.
  • 65
    Levites Y, Das P, Price RW, Rochette MJ, Kostura LA, McGowan EM, Murphy MP & Golde TE (2006) Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse model. J Clin Invest 116, 193201.