References
- Mattson MP. Pathways towards and away from Alzheimer's disease. Nature430, 631–639 (2004).
- Perry G, Rizzuto N, Autilio-Gambetti L, Gambetti P. Paired helical filaments from Alzheimer disease patients contain cytoskeletal components. Proc. Natl Acad. Sci. USA82, 3916–3920 (1985).
- Bartus RT, Dean RL 3rd, Beer B, Lippa AS. The cholinergic hypothesis of geriatric memory dysfunction. Science217, 408–414 (1982).
- Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease. Annu. Rev. Med.57, 513 (2005).
- Birks JS, Melzer D. Donepezil for mild and moderate Alzheimer's disease. Cochrane Database Syst. Rev.CD001190 (2000).
- Birks J, Iakovidou V, Tsolaki M. Rivastigmine for Alzheimer's disease. Cochrane Database Syst. Rev.CD001191 (2000).
- Olin J, Schneider L. Galantamine for Alzheimer's disease. Cochrane Database Syst. Rev.CD001747 (2002).
- Takeda A, Loveman E, Clegg A et al. A systematic review of the clinical effectiveness of donepezil, rivastigmine and galantamine on cognition, quality of life and adverse events in Alzheimer's disease. Int. J. Geriatr. Psych.21, 17–28 (2006).
- Reisberg B, Doody R, Stoffler A et al. Memantine in moderate-to-severe Alzheimer's disease. N. Engl. J. Med.348, 1333–1341 (2003).
- Farlow MR, Tariot P, Grossberg GT et al. Memantine/donepezil dual therapy is superior to placebo/donepezil therapy for treatment of moderate-to-severe Alzheimer's disease. Neurology60, A412 (2003).
- Areosa SA, Sherriff F, McShane R. Memantine for dementia. Cochrane Database Syst. Rev.CD003154 (2005).
- Josien H. Recent advances in the development of γ-secretase inhibitors. Curr. Opin. Drug Discov. Devel.5, 513–525 (2002).
- Dovey HF, John V, Anderson JP et al. Functional γ-secretase inhibitors reduce β-amyloid peptide levels in brain. J. Neurochem.76, 173–181 (2001).
- Das I, Craig C, Funahashi Y et al. Notch oncoproteins depend on γ-secretase/presenilin activity for processing and function. J. Biol. Chem.279, 30771–30780 (2004).
- Louvi A, Sisodia SS, Grove EA. Presenilin 1 in migration and morphogenesis in the central nervous system. Development131, 3093–3105 (2004).
- Tournoy J, Bossuyt X, Snellinx A et al. Partial loss of presenilins causes seborrheic keratosis and autoimmune disease in mice. Hum. Mol. Genet.13, 1321–1331 (2004).
- Wong GT, Manfra D, Poulet FM et al. Chronic treatment with the γ-secretase inhibitor LY-411,575 inhibits β-amyloid peptide production and alters lymphopoiesis and intestinal cell differentiation. J. Biol. Chem.279, 12876–12882 (2004).
- De Strooper B, Annaert W, Cupers P et al. A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain. Nature398, 518–522 (1999).
- Shen J, Bronson RT, Chen DF et al. Skeletal and CNS defects in Presenilin-1-deficient mice. Cell89, 629–639 (1997).
- Song W, Nadeau P, Yuan M et al. Proteolytic release and nuclear translocation of Notch-1 are induced by presenilin-1 and impaired by pathogenic presenilin-1 mutations. Proc. Natl Acad. Sci. USA96, 6959–6963 (1999).
- Handler M, Yang X, Shen J. Presenilin-1 regulates neuronal differentiation during neurogenesis. Development127, 2593–2606 (2000).
- Steiner H, Duff K, Capell A et al. A loss of function mutation of presenilin-2 interferes with amyloid β-peptide production and notch signaling. J. Biol. Chem.274, 28669–28673 (1999).
- Herreman A, Hartmann D, Annaert W et al. Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency. Proc. Natl Acad. Sci. USA96, 11872–11877 (1999).
- Donoviel DB, Hadjantonakis AK, Ikeda M et al. Mice lacking both presenilin genes exhibit early embryonic patterning defects. Genes Dev.13, 2801–2810 (1999).
- Feng R, Wang H, Wang J et al. Forebrain degeneration and ventricle enlargement caused by double knockout of Alzheimer's presenilin-1 and presenilin-2. Proc. Natl Acad. Sci. USA101, 8162–8167 (2004).
- Kim HS, Park CH, Cha SH et al. Carboxyl-terminal fragment of Alzheimer's APP destabilizes calcium homeostasis and renders neuronal cells vulnerable to excitotoxicity. FASEB J.14, 1508–1517 (2000).
- Siemers ER, Quinn JF, Kaye J et al. Effects of a γ-secretase inhibitor in a randomized study of patients with Alzheimer disease. Neurology66, 602–604 (2006).
- Vassar R, Bennett BD, Babu-Khan S et al. Χ-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. Science286, 735–741 (1999).
- Sinha S, Anderson JP, Barbour R et al. Purification and cloning of amyloid precursor protein β-secretase from human brain. Nature402, 537–540 (1999).
- Yan R, Bienkowski MJ, Shuck ME et al. Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity. Nature402, 533–537 (1999).
- Lin X, Koelsch G, Wu S et al. Human aspartic protease memapsin 2 cleaves the β-secretase site of β-amyloid precursor protein. Proc. Natl Acad. Sci. USA97, 1456–1460 (2000).
- Vassar R, Citron M. Aβ-generating enzymes: recent advances in β- and γ-secretase research. Neuron27, 419–422 (2000).
- Ghosh AK, Bilcer G, Harwood C et al. Structure-based design: potent inhibitors of human brain memapsin 2 (β-secretase). J. Med. Chem.44, 2865–2868 (2001).
- Hong L, Koelsch G, Lin X et al. Structure of the protease domain of memapsin 2 (β-secretase) complexed with inhibitor. Science290, 150–153 (2000).
- Francotte P, Graindorge E, Boverie S, de Tullio P, Pirotte B. New trends in the design of drugs against Alzheimer's disease. Curr. Med. Chem.11, 1757–1778 (2004).
- Steinhilb ML, Turner RS, Gaut JR. The protease inhibitor, MG132, blocks maturation of the amyloid precursor protein Swedish mutant preventing cleavage by β-Secretase. J. Biol. Chem.276, 4476–4484 (2001).
- Roberds SL, Anderson J, Basi G et al. BACE knockout mice are healthy despite lacking the primary β-secretase activity in brain: implications for Alzheimer's disease therapeutics. Hum. Mol. Genet.10, 1317–1324 (2001).
- Dominguez D, Tournoy J, Hartmann D et al. Phenotypic and biochemical analyses of BACE1- and BACE2-deficient mice. J. Biol. Chem.280, 30797–30806 (2005).
- Laird FM, Cai H, Savonenko AV 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).
- Jarvik GP, Wijsman EM, Kukull WA et al. Interactions of apolipoprotein E genotype, total cholesterol level, age, and sex in prediction of Alzheimer's disease: a case-control study. Neurology45, 1092–1096 (1995).
- Bales KR, Verina T, Dodel RC et al. Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition. Nat. Genet.17, 263–264 (1997).
- Fassbender K, Simons M, Bergmann C et al. Simvastatin strongly reduces levels of Alzheimer's disease β -amyloid peptides Aβ42 and Aβ 40in vivo and in vivo. Proc. Natl Acad. Sci. USA98, 5856–5861 (2001).
- Refolo LM, Pappolla MA, LaFrancois J et al. A cholesterol-lowering drug reduces β-amyloid pathology in a transgenic mouse model of Alzheimer's disease. Neurobiol. Dis.8, 890–899 (2001).
- Golde TE, Eckman CB. Cholesterol modulation as an emerging strategy for the treatment of Alzheimer's disease. Drug Discov. Today6, 1049–1055 (2001).
- Wolozin B, Kellman W, Ruosseau P, Celesia GG, Siegel G. Decreased prevalence of Alzheimer disease associated with 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitors. Arch. Neurol.57, 1439–1443 (2000).
- Shepherd J, Blauw GJ, Murphy MB et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet360, 1623–1630 (2002).
- Schenk D, Barbour R, Dunn W et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature400, 173–177 (1999).
- Games D, Bard F, Grajeda H et al. Prevention and reduction of AD-type pathology in PDAPP mice immunized with Aβ1–42. Ann NY Acad Sci920, 274–284 (2000).
- Bacskai BJ, Kajdasz ST, Christie RH et al. Imaging of amyloid-β deposits in brains of living mice permits direct observation of clearance of plaques with immunotherapy. Nat. Med.7, 369–372 (2001).
- Janus C. Vaccines for Alzheimer's disease: how close are we? CNS Drugs17, 457–474 (2003).
- Buttini M, Masliah E, Barbour R et al. Χ-amyloid immunotherapy prevents synaptic degeneration in a mouse model of Alzheimer's disease. J. Neurosci.25, 9096–9101 (2005).
- Oddo S, Billings L, Kesslak JP, Cribbs DH, LaFerla FM. Aβ immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome. Neuron43, 321–332 (2004).
- Bard F, Cannon C, Barbour R et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nat. Med.6, 916–919 (2000).
- Bard F, Barbour R, Cannon C et al. Epitope and isotype specificities of antibodies to β-amyloid peptide for protection against Alzheimer's disease-like neuropathology. Proc. Natl Acad. Sci. USA100, 2023–2028 (2003).
- Das P, Howard V, Loosbrock N et al. Amyloid-β immunization effectively reduces amyloid deposition in FcRγ-/- knock-out mice. J. Neurosci.23, 8532–8538 (2003).
- Bacskai BJ, Kajdasz ST, McLellan ME et al. Non-Fc-mediated mechanisms are involved in clearance of amyloid-β in vivo by immunotherapy. J. Neurosci.22, 7873–7878 (2002).
- McLaurin J, Cecal R, Kierstead ME et al. Therapeutically effective antibodies against amyloid-β peptide target amyloid-β residues 4–10 and inhibit cytotoxicity and fibrillogenesis. Nat. Med.8, 1263–1269 (2002).
- Dodart JC, Bales KR, Gannon KS et al. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nat. Neurosci.5, 452–457 (2002).
- DeMattos RB, Bales KR, Cummins DJ et al. Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease. Proc. Natl Acad. Sci. USA98, 8850–8855 (2001).
- Dodel RC, Du Y, Depboylu C et al. Intravenous immunoglobulins containing antibodies against β-amyloid for the treatment of Alzheimer's disease. J. Neurol. Neurosurg. Psych.75, 1472–1474 (2004).
- Dodel R, Hampel H, Depboylu C et al. Human antibodies against amyloid β peptide: a potential treatment for Alzheimer's disease. Ann. Neurol.52, 253–256 (2002).
- Hock C, Konietzko U, Streffer JR et al. Antibodies against β-amyloid slow cognitive decline in Alzheimer's disease. Neuron38, 547–554 (2003).
- Monsonego A, Weiner HL. Immunotherapeutic approaches to Alzheimer's disease. Science302, 834–838 (2003).
- Ferrer I, Boada Rovira M, Sanchez Guerra ML, Rey MJ, Costa-Jussa F. Neuropathology and pathogenesis of encephalitis following amyloid-β immunization in Alzheimer's disease. Brain Pathol.14, 11–20 (2004).
- Dodel RC, Hampel H, Du Y. Immunotherapy for Alzheimer's disease. Lancet Neurol.2, 215–220 (2003).
- Fox NC, Black RS, Gilman S et al. Effects of Aβ immunization (AN1792) on MRI measures of cerebral volume in Alzheimer disease. Neurology64, 1563–1572 (2005).
- Pfeifer M, Boncristiano S, Bondolfi L et al. Cerebral hemorrhage after passive anti-Aβ immunotherapy. Science298, 1379 (2002).
- Lee EB, Leng LZ, Lee VM, Trojanowski JQ. Meningoencephalitis associated with passive immunization of a transgenic murine model of Alzheimer's amyloidosis. FEBS Lett.579, 2564–2568 (2005).
- Gong Y, Chang L, Viola KL et al. Alzheimer's disease-affected brain: presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss. Proc. Natl Acad. Sci. USA100, 10417–10422 (2003).
- Chan SL, Griffin WS, Mattson MP. Evidence for caspase-mediated cleavage of AMPA receptor subunits in neuronal apoptosis and Alzheimer's disease. J. Neurosci. Res.57, 315–323 (1999).
- Kontush A, Berndt C, Weber W et al. Amyloid-β is an antioxidant for lipoproteins in cerebrospinal fluid and plasma. Free Radic. Biol. Med.30, 119–128 (2001).
- Zou K, Gong JS, Yanagisawa K, Michikawa M. A novel function of monomeric amyloid β-protein serving as an antioxidant molecule against metal-induced oxidative damage. J. Neurosci.22, 4833–4841 (2002).
- Gibson GE, Park LC, Sheu KF, Blass JP, Calingasan NY. The α-ketoglutarate dehydrogenase complex in neurodegeneration. Neurochem. Int.36, 97–112 (2000).
- Bursztajn S, DeSouza R, McPhie DL et al. Overexpression in neurons of human presenilin-1 or a presenilin-1 familial Alzheimer disease mutant does not enhance apoptosis. J. Neurosci.18, 9790–9799 (1998).
- Leutner S, Czech C, Schindowski K et al. Reduced antioxidant enzyme activity in brains of mice transgenic for human presenilin-1 with single or multiple mutations. Neurosci. Lett.292, 87–90 (2000).
- Andorn AC, Kalaria RN. Factors Affecting pro- and anti-oxidant properties of fragments of the b-protein precursor (bpp): implication for Alzheimer's disease. J. Alzheimers Dis.2, 69–78 (2000).
- Moreira PI, Smith MA, Zhu X et al. Therapeutic potential of oxidant mechanisms in Alzheimer disease. Expert Rev. Neurotherapeutics4, 995–1004 (2004).
- Smith MA, Atwood CS, Joseph JA, Perry G. Predicting the failure of amyloid-β vaccine. Lancet359, 1864–1865 (2002).
- Perry G, Nunomura A, Raina AK, Smith MA. Amyloid-β junkies. Lancet355, 757 (2000).
- Neuroinflammation Working Group. Inflammation and Alzheimer's disease. Neurobiol. Aging21, 383–421 (2000).
- Pratico D, Trojanowski JQ. Inflammatory hypotheses: novel mechanisms of Alzheimer's neurodegeneration and new therapeutic targets? Neurobiol. Aging21, 441–445 (2000).
- Weggen S, Eriksen JL, Das P et al. A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity. Nature414, 212–216 (2001).
- Gasparini L, Rusconi L, Xu H, del Soldato P, Ongini E. Modulation of β-amyloid metabolism by non-steroidal anti-inflammatory drugs in neuronal cell cultures. J. Neurochem.88, 337–348 (2004).
- Kukar T, Murphy MP, Eriksen JL et al. Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Aβ42 production. Nat. Med.11, 545–550 (2005).
- Eriksen JL, Sagi SA, Smith TE et al. NSAIDs and enantiomers of flurbiprofen target γ-secretase and lower Aβ 42in vivo. J. Clin. Invest.112, 440–449 (2003).
- Szekely CA, Thorne JE, Zandi PP et al. Nonsteroidal anti-inflammatory drugs for the prevention of Alzheimer's disease: a systematic review. Neuroepidemiology23, 159–169 (2004).
- Aisen PS, Schmeidler J, Pasinetti GM. Randomized pilot study of nimesulide treatment in Alzheimer's disease. Neurology58, 1050–1054 (2002).
- Aisen PS, Schafer KA, Grundman M et al. Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. JAMA289, 2819–2826 (2003).
- Reines SA, Block GA, Morris JC et al. Rofecoxib: no effect on Alzheimer's disease in a 1-year, randomized, blinded, controlled study. Neurology62, 66–71 (2004).
- Townsend KP, Pratico D. Novel therapeutic opportunities for Alzheimer's disease: focus on nonsteroidal anti-inflammatory drugs. FASEB J.19, 1592–1601 (2005).
- Cholerton B, Gleason CE, Baker LD, Asthana S. Estrogen and Alzheimer's disease: the story so far. Drugs Aging19, 405–427 (2002).
- Asthana S, Baker LD, Craft S et al. High-dose estradiol improves cognition for women with AD: results of a randomized study. Neurology57, 605–612 (2001).
- Baker LD, Sambamurti K, Craft S et al. 17β-estradiol reduces plasma Aβ40 for HRT-naive postmenopausal women with Alzheimer disease: a preliminary study. Am. J. Geriatr. Psych.11, 239–244 (2003).
- Geerlings MI, Launer LJ, de Jong FH et al. Endogenous estradiol and risk of dementia in women and men: the Rotterdam Study. Ann. Neurol.53, 607–615 (2003).
- Thal LJ, Thomas RG, Mulnard R et al. Estrogen levels do not correlate with improvement in cognition. Arch. Neurol.60, 209–212 (2003).
- Pinkerton JV, Henderson VW. Estrogen and cognition, with a focus on Alzheimer's disease. Semin. Reprod. Med.23, 172–179 (2005).
- Rapp SR, Espeland MA, Shumaker SA et al. Effect of estrogen plus progestin on global cognitive function in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA289, 2663–2672 (2003).
- Webber KM, Casadesus G, Marlatt MW et al. Estrogen bows to a new master: the role of gonadotropins in Alzheimer pathogenesis. Ann. NY Acad. Sci.1052, 201–209 (2005).
- Perry G, Castellani RJ, Smith MA et al. Oxidative damage in the olfactory system in Alzheimer's disease. Acta. Neuropathol.106, 552–556 (2003).
- Ghanbari HA, Ghanbari K, Harris PL et al. Oxidative damage in cultured human olfactory neurons from Alzheimer's disease patients. Aging Cell3, 41–44 (2004).
- Migliore L, Fontana I, Trippi F et al. Oxidative DNA damage in peripheral leukocytes of mild cognitive impairment and AD patients. Neurobiol. Aging26, 567–573 (2005).
- Nunomura A, Perry G, Aliev G et al. Oxidative damage is the earliest event in Alzheimer disease. J. Neuropathol. Exp. Neurol.60, 759–767 (2001).
- Honda K, Smith MA, Zhu X et al. Ribosomal RNA in Alzheimer disease is oxidized by bound redox-active iron. J. Biol. Chem.280, 20978–20986 (2005).
- Gutzmann H, Hadler D. Sustained efficacy and safety of idebenone in the treatment of Alzheimer's disease: update on a 2-year double-blind multicentre study. J. Neural. Transm.54, 301–310 (1998).
- Weyer G, Babej-Dolle RM, Hadler D, Hofmann S, Herrmann WM. A controlled study of 2 doses of idebenone in the treatment of Alzheimer's disease. Neuropsychobiology36, 73–82 (1997).
- Gutzmann H, Kuhl KP, Hadler D, Rapp MA. Safety and efficacy of idebenone versus tacrine in patients with Alzheimer's disease: results of a randomized, double-blind, parallel-group multicenter study. Pharmacopsychiatry35, 12–18 (2002).
- Thal LJ, Grundman M, Berg J et al. Idebenone treatment fails to slow cognitive decline in Alzheimer's disease. Neurology61, 1498–1502 (2003).
- Suh JH, Wang H, Liu RM, Liu J, Hagen TM. (R)-α-lipoic acid reverses the age-related loss in GSH redox status in post-mitotic tissues: evidence for increased cysteine requirement for GSH synthesis. Arch. Biochem. Biophys.423, 126–135 (2004).
- Hager K, Marahrens A, Kenklies M, Riederer P, Munch G. Α-lipoic acid as a new treatment option for Azheimer type dementia. Arch. Gerontol. Geriatr.32, 275–282 (2001).
- Frolich L, Gotz ME, Weinmuller M et al. (r)-, but not (s)-α lipoic acid stimulates deficient brain pyruvate dehydrogenase complex in vascular dementia, but not in Alzheimer dementia. J. Neural. Transm.111, 295–310 (2004).
- Bianchetti A, Rozzini R, Trabucchi M. Effects of acetyl-L-carnitine in Alzheimer's disease patients unresponsive to acetylcholinesterase inhibitors. Curr. Med. Res. Opin.19, 350–353 (2003).
- Montgomery SA, Thal LJ, Amrein R. Meta-analysis of double blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer's disease. Int. Clin. Psychopharmacol.18, 61–71 (2003).
- Hudson S, Tabet N. Acetyl-L-carnitine for dementia. Cochrane Database Syst. Rev.CD003158 (2003).
- Sano M, Ernesto C, Thomas RG et al. A controlled trial of selegiline, α-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N. Engl. J. Med.336, 1216–1222 (1997).
- Grundman M. Vitamin E and Alzheimer disease: the basis for additional clinical trials. Am. J. Clin. Nutr.71, S630–S636 (2000).
- Engelhart MJ, Geerlings MI, Ruitenberg A et al. Dietary intake of antioxidants and risk of Alzheimer disease. JAMA287, 3223–3229 (2002).
- Morris MC, Evans DA, Bienias JL et al. Dietary intake of antioxidant nutrients and the risk of incident Alzheimer disease in a biracial community study. JAMA287, 3230–3237 (2002).
- Zandi PP, Anthony JC, Khachaturian AS et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. Arch. Neurol.61, 82–88 (2004).
- Petersen RC, Thomas RG, Grundman M et al. Vitamin E and donepezil for the treatment of mild cognitive impairment. N. Engl. J. Med.352, 2379–2388 (2005).
- Luchsinger JA, Tang MX, Shea S, Mayeux R. Antioxidant vitamin intake and risk of Alzheimer disease. Arch. Neurol.60, 203–208 (2003).
- Laurin D, Masaki KH, Foley DJ, White LR, Launer LJ. Midlife dietary intake of antioxidants and risk of late-life incident dementia: the Honolulu-Asia Aging Study. Am. J. Epidemiol.159, 959–967 (2004).
- Stackman RW, Eckenstein F, Frei B et al. Prevention of age-related spatial memory deficits in a transgenic mouse model of Alzheimer's disease by chronic Ginkgo biloba treatment. Exp. Neurol.184, 510–520 (2003).
- Yao ZX, Han Z, Drieu K, Papadopoulos V. Ginkgo biloba extract (Egb 761) inhibits β-amyloid production by lowering free cholesterol levels. J. Nutr. Biochem.15, 749–756 (2004).
- Le Bars PL, Katz MM, Berman N et al. A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group. JAMA278, 1327–1332 (1997).
- Smith MA, Harris PL, Sayre LM, Perry G. Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. Proc. Natl Acad. Sci. USA94, 9866–9868 (1997).
- Sayre LM, Perry G, Harris PL et al. In situ oxidative catalysis by neurofibrillary tangles and senile plaques in Alzheimer's disease: a central role for bound transition metals. J. Neurochem.74, 270–279 (2000).
- Raman B, Ban T, Yamaguchi K et al. Metal ion-dependent effects of clioquinol on the fibril growth of an amyloid {β} peptide. J. Biol. Chem.280, 16157–16162 (2005).
- Cherny RA, Atwood CS, Xilinas ME et al. Treatment with a copper-zinc chelator markedly and rapidly inhibits β-amyloid accumulation in Alzheimer's disease transgenic mice. Neuron30, 665–676 (2001).
- Ritchie CW, Bush AI, Mackinnon A et al. Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Aβ amyloid deposition and toxicity in Alzheimer disease: a pilot Phase II clinical trial. Arch. Neurol.60, 1685–1691 (2003).
- Ibach B, Haen E, Marienhagen J, Hajak G. Clioquinol treatment in familiar early onset of Alzheimer's disease: a case report. Pharmacopsychiatry38, 178–179 (2005).
- Casadesus G, Atwood CS, Zhu X et al. Evidence for the role of gonadotropin hormones in the development of Alzheimer disease. Cell Mol. Life Sci.62, 293–298 (2005).
- Webber KM, Casadesus G, Zhu X et al. The cell cycle and hormonal fluxes in Alzheimer disease: a novel therapeutic target. Curr. Pharm. Des.12, 691–697 (2006).
- Casadesus G, Webber KM, Atwood CS et al. Luteinizing hormone modulates cognition and amyloid-β deposition in Alzheimer APP transgenic mice. Biochim. Biophys. Acta.1762, 447–452 (2006).
- Smith MA, Casadesus G, Joseph JA, Perry G. Amyloid-β and tau serve antioxidant functions in the aging and Alzheimer brain. Free Radic. Biol. Med.33, 1194–1199 (2002).
- Perry G, Taddeo MA, Nunomura A et al. Comparative biology and pathology of oxidative stress in Alzheimer and other neurodegenerative diseases: beyond damage and response. Comp. Biochem. Physiol. C Toxicol Pharmacol.133, 507–513 (2002).
- Nunomura A, Perry G, Pappolla MA et al. Neuronal oxidative stress precedes amyloid-β deposition in Down syndrome. J. Neuropathol. Exp. Neurol.59, 1011–1017 (2000).
- Nunomura A, Perry G, Pappolla MA et al. RNA oxidation is a prominent feature of vulnerable neurons in Alzheimer's disease. J. Neurosci.19, 1959–1964 (1999).
- Smith MA, Richey Harris PL, Sayre LM, Beckman JS, Perry G. Widespread peroxynitrite-mediated damage in Alzheimer's disease. J. Neurosci.17, 2653–2657 (1997).
- Cras P, Smith MA, Richey PL et al. Extracellular neurofibrillary tangles reflect neuronal loss and provide further evidence of extensive protein cross-linking in Alzheimer disease. Acta. Neuropathol.89, 291–295 (1995).
- Sayre LM, Zelasko DA, Harris PL et al. 4-Hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer's disease. J. Neurochem.68, 2092–2097 (1997).
- Zhu X, Raina AK, Lee HG et al. Oxidative stress signalling in Alzheimer's disease. Brain Res.1000, 32–39 (2004).
- Liu Q, Smith MA, Avila J et al. Alzheimer-specific epitopes of tau represent lipid peroxidation-induced conformations. Free Radic. Biol. Med.38, 746–754 (2005).
- Castellani RJ, Harris PL, Sayre LM et al. Active glycation in neurofibrillary pathology of Alzheimer disease: N(ε)-(carboxymethyl) lysine and hexitol-lysine. Free Radic. Biol. Med.31, 175–180 (2001).
- Scarmeas N, Stern Y, Tang MX, Mayeux R, Luchsinger JA. Mediterranean diet and risk for Alzheimer's disease. Ann. Neurol. (2006) (Epub ahead of print).
Websites
- Official neurochem site www.neurochem.com
- Clinicaltrials.gov www.clinicaltrials.gov