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Review

Distinguishing Lewy body dementias from Alzheimer’s disease

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Pages 1499-1516 | Published online: 09 Jan 2014

References

  • Galvin JE, Pollack J, Morris JC. Clinical phenotype of Parkinson disease dementia. Neurology67(9), 1605–1611 (2006).
  • Aarsland D, Andersen K, Larsen JP, Lolk A, Kragh-Sorensen P. Prevalence and characteristics of dementia in Parkinson disease: an 8-year prospective study. Arch. Neurol.60(3), 387–392 (2003).
  • Aarsland D, Andersen K, Larsen JP, Lolk A, Nielsen H, Kragh-Sorensen P. Risk of dementia in Parkinson’s disease: a community-based, prospective study. Neurology56(6), 730–736 (2001).
  • Galvin JE, Lee VM, Trojanowski JQ. Synucleinopathies: clinical and pathological implications. Arch. Neurol.58(2), 186–190 (2001).
  • Galvin JE. Dementia with Lewy bodies. Arch. Neurol.60(9), 1332–1335 (2003).
  • McKeith IG, Dickson DW, Lowe J et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology65(12), 1863–1872 (2005).
  • Johnson DK, Morris JC, Galvin JE. Verbal and visuospatial deficits in dementia with Lewy bodies. Neurology65(8), 1232–1238 (2005).
  • Lippa CF, Duda JE, Grossman M et al. DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology68(11), 812–819 (2007).
  • Barker WW, Luis CA, Kashuba A et al. Relative frequencies of Alzheimer disease, Lewy body, vascular and frontotemporal dementia, and hippocampal sclerosis in the State of Florida Brain Bank. Alzheimer Dis. Assoc. Disord.16(4), 203–212 (2002).
  • Hughes TA, Ross HF, Musa S et al. A 10-year study of the incidence of and factors predicting dementia in Parkinson’s disease. Neurology54(8), 1596–1602 (2000).
  • Schrag A, Jahanshahi M, Quinn N. What contributes to quality of life in patients with Parkinson’s disease? J. Neurol. Neurosurg. Psychiatr.69(3), 308–312 (2000).
  • Aarsland D, Larsen JP, Tandberg E, Laake K. Predictors of nursing home placement in Parkinson’s disease: a population-based, prospective study. J. Am. Geriatr. Soc.48(8), 938–942 (2000).
  • Diagnostic and Statistical Manual of Mental Disorders IV (4th Edition). American Psychiatric Association. DC, USA (1994).
  • McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s Disease. Neurology34(7), 939–944 (1984).
  • Dubois B, Feldman HH, Jacova C et al. Research criteria for the diagnosis of Alzheimer’s disease: revising the NINCDS-ADRDA criteria. Lancet Neurol.6(8), 734–746 (2007).
  • Litvan I, MacIntyre A, Goetz CG et al. Accuracy of the clinical diagnoses of Lewy body disease, Parkinson disease, and dementia with Lewy bodies: a clinicopathologic study. Arch. Neurol.55(7), 969–978 (1998).
  • McKeith IG, Ballard CG, Perrry RH et al. Prospective validation of consensus criteria for the diagnosis of dementia with Lewy bodies. Neurology54(5), 1050–1058 (2000).
  • Galasko D. Cerebrospinal fluid biomarkers in Alzheimer disease: a fractional improvement? Arch. Neurol.60(9), 1195–1196 (2003).
  • Balsis S, Carpenter BD, Storandt M. Personality change precedes clinical diagnosis of dementia of the Alzheimer type. J. Gerontol.60(2), P98–P101 (2005).
  • Oppenheim G. The earliest signs of Alzheimer’s disease. J. Geriatr. Psychiatry Neurol.7(2), 116–120 (1994).
  • Wild KV, Kaye JA, Oken BS. Early noncognitive change in Alzheimer’s disease and healthy aging. J. Geriatr. Psychiatry Neurol.7(4), 199–205 (1994).
  • McKeith I, Fairbairn A, Perry R, Thompson P, Perry E. Neuroleptic sensitivity in patients with senile dementia of Lewy body type. Br. Med. J.305(6855), 673–678 (1992).
  • McKeith IG, Perry RH, Fairbairn AF, Jabeen S, Perry EK. Operational criteria for senile dementia of Lewy body type (SDLT). Psychol. Med.22(4), 911–922 (1992).
  • Stavitsky K, Brickman AM, Scarmeas N et al. The progression of cognition, psychiatric symptoms, and functional abilities in dementia with Lewy bodies and Alzheimer disease. Arch. Neurol.63(10), 1450–1456 (2006).
  • Weiner MF, Hynan LS, Parikh B et al. Can Alzheimer’s disease and dementias with Lewy bodies be distinguished clinically? J. Geriatr. Psychiatry Neurol.16(4), 245–250 (2003).
  • Gibb WR, Luthert PJ, Janota I, Lantos PL. Cortical Lewy body dementia: clinical features and classification. J. Neurol. Neurosurg. Psychiatr.52(2), 185–192 (1989).
  • Olichney JM, Galasko D, Salmon DP et al. Cognitive decline is faster in Lewy body variant than in Alzheimer’s disease. Neurology51(2), 351–357 (1998).
  • Walker Z, Allen RL, Shergill S, Mullan E, Katona CL. Three years survival in patients with a clinical diagnosis of dementia with Lewy bodies. Int. J. Geriatr. Psychiatry15(3), 267–273 (2000).
  • Tiraboschi P, Salmon DP, Hansen LA, Hofstetter RC, Thal LJ, Corey-Bloom J. What best differentiates Lewy body from Alzheimer’s disease in early-stage dementia? Brain129(Pt 3), 729–735 (2006).
  • Devanand DP, Jacobs DM, Tang MX et al. The course of psychopathologic features in mild to moderate Alzheimer disease. Arch. Gen. Psychiatry54(3), 257–263 (1997).
  • Lopez OL, Wisniewski S, Hamilton RL, Becker JT, Kaufer DI, DeKosky ST. Predictors of progression in patients with AD and Lewy bodies. Neurology54(9), 1774–1779 (2000).
  • Williams MM, Xiong C, Morris JC, Galvin JE. Survival and mortality differences between dementia with Lewy bodies vs Alzheimer disease. Neurology67(11), 1935–1941 (2006).
  • Roos RA, Jongen JC, van der Velde EA. Clinical course of patients with idiopathic Parkinson’s disease. Mov. Disord.11(3), 236–242 (1996).
  • Merdes AR, Hansen LA, Jeste DV et al. Influence of Alzheimer pathology on clinical diagnostic accuracy in dementia with Lewy bodies. Neurology60(10), 1586–1590 (2003).
  • Galasko D, Katzman R, Salmon DP, Hansen L. Clinical and neuropathological findings in Lewy body dementias. Brain Cogn31(2), 166–175 (1996).
  • Salmon DP, Galasko D, Hansen LA et al. Neuropsychological deficits associated with diffuse Lewy body disease. Brain Cogn31(2), 148–165 (1996).
  • Strauss ME, Pasupathi M, Chatterjee A. Concordance between observers in descriptions of personality change in Alzheimer’s disease. Psychol. Aging8(4), 475–480 (1993).
  • Siegler IC, Dawson DV, Welsh KA. Caregiver ratings of personality change in Alzheimer’s disease patients: a replication. Psychol. Aging9(3), 464–466 (1994).
  • Rubin EH, Morris JC, Berg L. The progression of personality changes in senile dementia of the Alzheimer’s type. J. Am. Geriatr. Soc.35(8), 721–725 (1987).
  • Bozzola FG, Gorelick PB, Freels S. Personality changes in Alzheimer’s disease. Arch. Neurol.49(3), 297–300 (1992).
  • Barber R, Snowden JS, Craufurd D. Frontotemporal dementia and Alzheimer’s disease: retrospective differentiation using information from informants. J. Neurol. Neurosurg. Psychiatr.59(1), 61–70 (1995).
  • Mychack P, Rosen H, Miller BL. Novel applications of social-personality measures to the study of dementia. Neurocase7(2), 131–143 (2001).
  • Golden Z, Golden CJ. The differential impacts of Alzheimer’s dementia, head injury, and stroke on personality dysfunction. Int. J. Neurosci.113(6), 869–878 (2003).
  • Galvin JE, Malcom H, Johnson D, Morris JC. Personality traits distinguishing dementia with Lewy bodies from Alzheimer disease. Neurology68(22), 1895–1901 (2007).
  • Marti MJ, Tolosa E, Campdelacreu J. Clinical overview of the synucleinopathies. Mov. Disord.18(Suppl. 6), S21–S27 (2003).
  • Iranzo A, Santamaria J, Rye DB et al. Characteristics of idiopathic REM sleep behavior disorder and that associated with MSA and PD. Neurology65(2), 247–252 (2005).
  • Weisman D, Cho M, Taylor C, Adame A, Thal LJ, Hansen LA. In dementia with Lewy bodies, Braak stage determines phenotype, not Lewy body distribution. Neurology69(4), 356–359 (2007).
  • McKeith IG. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the Consortium on DLB International Workshop. J. Alzheimers Dis.9(Suppl. 3), 417–423 (2006).
  • Braak H, Alafuzoff I, Arzberger T, Kretzschmar H, Del Tredici K. Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol.112(4), 389–404 (2006).
  • Braak H, Rub U, Jansen Steur EN, Del Tredici K, de Vos RA. Cognitive status correlates with neuropathologic stage in Parkinson disease. Neurology64(8), 1404–1410 (2005).
  • Perry EK, Haroutunian V, Davis KL et al. Neocortical cholinergic activities differentiate Lewy body dementia from classical Alzheimer’s disease. Neuroreport5(7), 747–749 (1994).
  • Sabbagh MN, Corey-Bloom J, Tiraboschi P, Thomas R, Masliah E, Thal LJ. Neurochemical markers do not correlate with cognitive decline in the Lewy body variant of Alzheimer disease. Arch. Neurol.56(12), 1458–1461 (1999).
  • Tiraboschi P, Hansen LA, Alford M et al. Early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease. Arch. Gen. Psychiatry59(10), 946–951 (2002).
  • Tiraboschi P, Hansen LA, Alford M, Masliah E, Thal LJ, Corey-Bloom J. The decline in synapses and cholinergic activity is asynchronous in Alzheimer’s disease. Neurology55(9), 1278–1283 (2000).
  • Liberini P, Valerio A, Memo M, Spano PF. Lewy-body dementia and responsiveness to cholinesterase inhibitors: a paradigm for heterogeneity of Alzheimer’s disease? Trends Pharmacol. Sci.17(4), 155–160 (1996).
  • Gotti C, Moretti M, Bohr I et al. Selective nicotinic acetylcholine receptor subunit deficits identified in Alzheimer’s disease, Parkinson’s disease and dementia with Lewy bodies by immunoprecipitation. Neurobiol. Dis.23(2), 481–489 (2006).
  • Teaktong T, Graham AJ, Court JA et al. Nicotinic acetylcholine receptor immunohistochemistry in Alzheimer’s disease and dementia with Lewy bodies: differential neuronal and astroglial pathology. J. Neurol. Sci.225(1–2), 39–49 (2004).
  • Court JA, Ballard CG, Piggott MA et al. Visual hallucinations are associated with lower α bungarotoxin binding in dementia with Lewy bodies. Pharmacol. Biochem. Behav.70(4), 571–579 (2001).
  • Rei RT, Sabbagh MN, Corey-Bloom J, Tiraboschi P, Thal LJ. Nicotinic receptor losses in dementia with Lewy bodies: comparisons with Alzheimer’s disease. Neurobiol. Aging21(5), 741–746 (2000).
  • Walter J, Kaether C, Steiner H, Haass C. The cell biology of Alzheimer’s disease: uncovering the secrets of secretases. Curr. Opin. Neurobiol.11(5), 585–590 (2001).
  • Ohyagi Y, Asahara H, Chui DH et al. Intracellular Aβ42 activates p53 promoter: a pathway to neurodegeneration in Alzheimer’s disease. FASEB J.19(2), 255–257 (2005).
  • Kohler C, Ebert U, Baumann K, Schroder H. Alzheimer’s disease-like neuropathology of gene-targeted APP-SLxPS1mut mice expressing the amyloid precursor protein at endogenous levels. Neurobiol. Dis.20(2), 528–540 (2005).
  • Hull M, Berger M, Heneka M. Disease-modifying therapies in Alzheimer’s disease: how far have we come? Drugs66(16), 2075–2093 (2006).
  • Yoshimoto M, Iwai A, Kang D, Otero DA, Xia Y, Saitoh T. NACP, the precursor protein of the non-amyloid β/A4 protein (Aβ) component of Alzheimer disease amyloid, binds Aβ and stimulates Aβ aggregation. Proc. Natl Acad. Sci. USA92(20), 9141–9145 (1995).
  • Giacomelli CE, Norde W. Conformational changes of the amyloid β-peptide1–40 adsorbed on solid surfaces. Macromol. Biosci.5(5), 401–407 (2005).
  • Butterfield DA. Amyloid β-peptide1–42-associated free radical-induced oxidative stress and neurodegeneration in Alzheimer’s disease brain: mechanisms and consequences. Curr. Med. Chem.10(24), 2651–2659 (2003).
  • Bibl M, Mollenhauer B, Lewczuk P et al. Validation of amyloid-β peptides in CSF diagnosis of neurodegenerative dementias. Mol. Psychiatry12(7), 671–680 (2007).
  • Dong J, Atwood CS, Anderson VE et al. Metal binding and oxidation of amyloid-β within isolated senile plaque cores: Raman microscopic evidence. Biochemistry42(10), 2768–2773 (2003).
  • Bibl M, Mollenhauer B, Esselmann H et al. CSF amyloid-β-peptides in Alzheimer’s disease, dementia with Lewy bodies and Parkinson’s disease dementia. Brain129(Pt 5), 1177–1187 (2006).
  • Lippa CF, Ozawa K, Mann DM et al. Deposition of β-amyloid subtypes 40 and 42 differentiates dementia with Lewy bodies from Alzheimer disease. Arch. Neurol.56(9), 1111–1118 (1999).
  • Lippa CF, Nee LE, Mori H, St George-Hyslop P. Aβ-42 deposition precedes other changes in PS-1 Alzheimer’s disease. Lancet352(9134), 1117–1118 (1998).
  • Lippa CF. Synaptophysin immunoreactivity in Pick’s disease: comparison with Alzheimer’s disease and dementia with Lewy bodies. Am. J. Alzheimers Dis. Other Demen.19(6), 341–344 (2004).
  • Gomez-Tortosa E, Irizarry MC, Gomez-Isla T, Hyman BT. Clinical and neuropathological correlates of dementia with Lewy bodies. Ann. NY Acad. Sci.920, 9–15 (2000).
  • Samuel W, Alford M, Hofstetter CR, Hansen L. Dementia with Lewy bodies versus pure Alzheimer disease: differences in cognition, neuropathology, cholinergic dysfunction, and synapse density. J. Neuropathol. Exp. Neurol.56(5), 499–508 (1997).
  • Harding AJ, Broe GA, Halliday GM. Visual hallucinations in Lewy body disease relate to Lewy bodies in the temporal lobe. Brain125(Pt 2), 391–403 (2002).
  • Hansen LA, Masliah E, Galasko D, Terry RD. Plaque-only Alzheimer disease is usually the Lewy body variant, and vice versa. J. Neuropathol. Exp. Neurol.52(6), 648–654 (1993).
  • Spillantini MG, Crowther RA, Jakes R, Hasegawa M, Goedert M. α-synuclein in filamentous inclusions of Lewy bodies from Parkinson’s disease and dementia with lewy bodies. Proc. Natl Acad. Sci. USA95(11), 6469–6473 (1998).
  • Paleologou KE, Irvine GB, El-Agnaf OM. α-synuclein aggregation in neurodegenerative diseases and its inhibition as a potential therapeutic strategy. Biochem. Soc. Trans.33(Pt 5), 1106–1110 (2005).
  • Pandey N, Schmidt RE, Galvin JE. The α-synuclein mutation E46K promotes aggregation in cultured cells. Exp. Neurol.197(2), 515–520 (2006).
  • Uversky VN, Li J, Fink AL. Pesticides directly accelerate the rate of α-synuclein fibril formation: a possible factor in Parkinson’s disease. FEBS Lett.500(3), 105–108 (2001).
  • Uversky VN. What does it mean to be natively unfolded? Eur. J. Biochem.269(1), 2–12 (2002).
  • Uversky VN. A protein-chameleon: conformational plasticity of α-synuclein, a disordered protein involved in neurodegenerative disorders. J. Biomol. Struct. Dyn.21(2), 211–234 (2003).
  • Tan EK, Chai A, Teo YY et al. α-synuclein haplotypes implicated in risk of Parkinson’s disease. Neurology62(1), 128–131 (2004).
  • Farrer M, Maraganore DM, Lockhart P et al. α-synuclein gene haplotypes are associated with Parkinson’s disease. Hum. Mol. Genet.10(17), 1847–1851 (2001).
  • Singleton AB, Farrer M, Johnson J et al. α-Synuclein locus triplication causes Parkinson’s disease. Science302(5646), 841 (2003).
  • Uversky VN, Li J, Fink AL. Metal-triggered structural transformations, aggregation, and fibrillation of human α-synuclein. A possible molecular NK between Parkinson’s disease and heavy metal exposure. J. Biol. Chem.276(47), 44284–44296 (2001).
  • Polymeropoulos MH, Higgins JJ, Golbe LI et al. Mapping of a gene for Parkinson’s disease to chromosome 4q21-q23. Science274(5290), 1197–1199 (1996).
  • Kruger R, Kuhn W, Muller T et al. Ala30Pro mutation in the gene encoding α-synuclein in Parkinson’s disease. Nat. Genet.18(2), 106–108 (1998).
  • Zarranz JJ, Alegre J, Gomez-Esteban JC et al. The new mutation, E46K, of α-synuclein causes Parkinson and Lewy body dementia. Ann. Neurol.55(2), 164–173 (2004).
  • Dekker MC, Bonifati V, van Duijn CM. Parkinson’s disease: piecing together a genetic jigsaw. Brain126(Pt 8), 1722–1733 (2003).
  • Liu Y, Fallon L, Lashuel HA, Liu Z, Lansbury PT Jr. The UCH-L1 gene encodes two opposing enzymatic activities that affect α-synuclein degradation and Parkinson’s disease susceptibility. Cell111(2), 209–218 (2002).
  • Mizuno Y, Hattori N, Kitada T et al. Familial Parkinson’s disease. α-synuclein and parkin. Adv. Neurol.86, 13–21 (2001).
  • Moore DJ, Zhang L, Dawson TM, Dawson VL. A missense mutation (L166P) in DJ-1, linked to familial Parkinson’s disease, confers reduced protein stability and impairs homo-oligomerization. J. Neurochem.87(6), 1558–1567 (2003).
  • Valente EM, Abou-Sleiman PM, Caputo V et al. Hereditary early-onset Parkinson’s disease caused by mutations in PINK1. Science304(5674), 1158–1160 (2004).
  • West AB, Moore DJ, Biskup S et al. Parkinson’s disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity. Proc. Natl Acad. Sci. USA102(46), 16842–16847 (2005).
  • Lippa CF, Schmidt ML, Lee VM, Trojanowski JQ. Antibodies to α-synuclein detect Lewy bodies in many Down’s syndrome brains with Alzheimer’s disease. Ann. Neurol.45(3), 353–357 (1999).
  • Rosenberg CK, Pericak-Vance MA, Saunders AM, Gilbert JR, Gaskell PC, Hulette CM. Lewy body and Alzheimer pathology in a family with the amyloid-β precursor protein APP717 gene mutation. Acta Neuropathol.100(2), 145–152 (2000).
  • Rebeck GW, Harr SD, Strickland DK, Hyman BT. Multiple, diverse senile plaque-associated proteins are ligands of an apolipoprotein E receptor, the α2-macroglobulin receptor/low-density-lipoprotein receptor-related protein. Ann. Neurol.37(2), 211–217 (1995).
  • Kounnas MZ, Moir RD, Rebeck GW et al. LDL receptor-related protein, a multifunctional ApoE receptor, binds secreted β-amyloid precursor protein and mediates its degradation. Cell82(2), 331–340 (1995).
  • Borroni B, Grassi M, Costanzi C, Archetti S, Caimi L, Padovani A. APOE genotype and cholesterol levels in lewy body dementia and Alzheimer disease: investigating genotype–phenotype effect on disease risk. Am. J. Geriatr. Psychiatry14(12), 1022–1031 (2006).
  • Lippa CF, Smith TW, Saunders AM et al. Apolipoprotein E genotype and Lewy body disease. Neurology45(1), 97–103 (1995).
  • Sakai J, Hoshino A, Takahashi S et al. Structure, chromosome location, and expression of the human very low density lipoprotein receptor gene. J. Biol. Chem.269(3), 2173–2182 (1994).
  • Helbecque N, Amouyel P. Very low density lipoprotein receptor in Alzheimer disease. Microsc. Res. Tech.50(4), 273–277 (2000).
  • Rebeck GW, Reiter JS, Strickland DK, Hyman BT. Apolipoprotein E in sporadic Alzheimer’s disease: allelic variation and receptor interactions. Neuron11(4), 575–580 (1993).
  • Thal LJ, Rosen W, Sharpless NS, Crystal H. Choline chloride fails to improve cognition of Alzheimer’s disease. Neurobiol. Aging2(3), 205–208 (1981).
  • Etienne P, Dastoor D, Gauthier S, Ludwick R, Collier B. Alzheimer disease: lack of effect of lecithin treatment for 3 months. Neurology31(12), 1552–1554 (1981).
  • Mesulam MM, Geula C. Butyrylcholinesterase reactivity differentiates the amyloid plaques of aging from those of dementia. Ann. Neurol.36(5), 722–727 (1994).
  • Perry EK, Atack JR, Perry RH et al. Intralaminar neurochemical distributions in human midtemporal cortex: comparison between Alzheimer’s disease and the normal. J. Neurochem.42(5), 1402–1410 (1984).
  • Greig NH, Lahiri DK, Sambamurti K. Butyrylcholinesterase: an important new target in Alzheimer’s disease therapy. Int. Psychogeriatr.14(Suppl. 1), 77–91 (2002).
  • Knapp MJ, Knopman DS, Solomon PR, Pendlebury WW, Davis CS, Gracon SI. A 30-week randomized controlled trial of high-dose tacrine in patients with Alzheimer’s disease. The Tacrine Study Group. JAMA271(13), 985–991 (1994).
  • Raskind MA, Peskind ER, Wessel T, Yuan W. Galantamine in AD: A 6-month randomized, placebo-controlled trial with a 6-month extension. The Galantamine USA-1 Study Group. Neurology54(12), 2261–2268 (2000).
  • Trinh NH, Hoblyn J, Mohanty S, Yaffe K. Efficacy of cholinesterase inhibitors in the treatment of neuropsychiatric symptoms and functional impairment in Alzheimer disease: a meta-analysis. JAMA289(2), 210–216 (2003).
  • Lanctot KL, Herrmann N, Yau KK et al. Efficacy and safety of cholinesterase inhibitors in Alzheimer’s disease: a meta-analysis. CMAJ169(6), 557–564 (2003).
  • Rees TM, Brimijoin S. The role of acetylcholinesterase in the pathogenesis of Alzheimer’s disease. Drugs Today39(1), 75–83 (2003).
  • Ballard CG, Chalmers KA, Todd C et al. Cholinesterase inhibitors reduce cortical Aβ in dementia with Lewy bodies. Neurology68(20), 1726–1729 (2007).
  • Hock C, Maddalena A, Raschig A et al. Treatment with the selective muscarinic m1 agonist talsaclidine decreases cerebrospinal fluid levels of Aβ42 in patients with Alzheimer’s disease. Amyloid10(1), 1–6 (2003).
  • Hashimoto M, Kazui H, Matsumoto K, Nakano Y, Yasuda M, Mori E. Does donepezil treatment slow the progression of hippocampal atrophy in patients with Alzheimer’s disease? Am. J. Psychiatry162(4), 676–682 (2005).
  • Albuquerque EX, Santos MD, Alkondon M, Pereira EF, Maelicke A. Modulation of nicotinic receptor activity in the central nervous system: a novel approach to the treatment of Alzheimer disease. Alzheimer Dis. Assoc. Disord.15(Suppl. 1) S19–S25 (2001).
  • Samochocki M, Hoffle A, Fehrenbacher A et al. Galantamine is an allosterically potentiating ligand of neuronal nicotinic but not of muscarinic acetylcholine receptors. J. Pharmacol. Exp. Ther.305(3), 1024–1036 (2003).
  • Stahl SM. The new cholinesterase inhibitors for Alzheimer’s disease, Part 1: their similarities are different. J. Clin. Psychiatry61(10), 710–711 (2000).
  • Touchon J, Bergman H, Bullock R, Rapatz G, Nagel J, Lane R. Response to rivastigmine or donepezil in Alzheimer’s patients with symptoms suggestive of concomitant Lewy body pathology. Curr. Med. Res. Opin.22(1), 49–59 (2006).
  • Samuel W, Caligiuri M, Galasko D et al. Better cognitive and psychopathologic response to donepezil in patients prospectively diagnosed as dementia with Lewy bodies: a preliminary study. Int. J. Geriatr. Psychiatry15(9), 794–802 (2000).
  • Nordberg A, Svensson AL. Cholinesterase inhibitors in the treatment of Alzheimer’s disease: a comparison of tolerability and pharmacology. Drug Saf.19(6), 465–480 (1998).
  • Roesler M, Ackenheil M. An open study evaluating the efficacy and safety of rivastigmine in patients with mixed dementia. Presented at: 41st American College of Neuropsychopharmacology. Puerto Rico, 8–12 December (2002).
  • Gabelli C. Rivastigmine: an update on therapeutic efficacy in Alzheimer’s disease and other conditions. Curr. Med. Res. Opin.19(2), 69–82 (2003).
  • McKeith I, Del Ser T, Spano P et al. Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet356(9247), 2031–2036 (2000).
  • Grace J, Daniel S, Stevens T et al. Long-term use of rivastigmine in patients with dementia with Lewy bodies: an open-label trial. Int. Psychogeriatr.13(2), 199–205 (2001).
  • Rozzini L, Chilovi BV, Bertoletti E et al. Cognitive and psychopathologic response to rivastigmine in dementia with Lewy bodies compared to Alzheimer’s disease: a case control study. Am. J. Alzheimers Dis. Other Demen.22(1), 42–47 (2007).
  • Small GW, Rabins PV, Barry PP et al. Diagnosis and treatment of Alzheimer disease and related disorders. Consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer’s Association, and the American Geriatrics Society. JAMA278(16), 1363–1371 (1997).
  • Rogers SL, Doody RS, Mohs RC, Friedhoff LT. Donepezil improves cognition and global function in Alzheimer disease: a 15-week, double-blind, placebo-controlled study. Donepezil Study Group. Arch. Intern. Med.158(9), 1021–1031 (1998).
  • Mori S, Mori E, Iseki E, Kosaka K. Efficacy and safety of donepezil in patients with dementia with Lewy bodies: preliminary findings from an open-label study. Psychiatr. Clin. Neurosci.60(2), 190–195 (2006).
  • Tariot PN, Solomon PR, Morris JC, Kershaw P, Lilienfeld S, Ding C. A 5-month, randomized, placebo-controlled trial of galantamine in AD. The Galantamine USA-10 Study Group. Neurology54(12), 2269–2276 (2000).
  • MacGowan SH, Wilcock GK, Scott M. Effect of gender and apolipoprotein E genotype on response to anticholinesterase therapy in Alzheimer’s disease. Int. J. Geriatr. Psychiatry13(9), 625–630 (1998).
  • Edwards K, Royall D, Hershey L et al. Efficacy and safety of galantamine in patients with dementia with Lewy bodies: a 24-week open-label study. Dement. Geriatr. Cogn Disord.23(6), 401–405 (2007).
  • Court J, Spurden D, Lloyd S et al. Neuronal nicotinic receptors in dementia with Lewy bodies and schizophrenia: α-bungarotoxin and nicotine binding in the thalamus. J. Neurochem.73(4), 1590–1597 (1999).
  • Jann MW, Shirley KL, Small GW. Clinical pharmacokinetics and pharmacodynamics of cholinesterase inhibitors. Clin. Pharmacokinet.41(10), 719–739 (2002).
  • Fernandez HH, Wu CK, Ott BR. Pharmacotherapy of dementia with Lewy bodies. Expert Opin. Pharmacother.4(11), 2027–2037 (2003).
  • Parkinson Study Group. Pramipexole vs levodopa as initial treatment for Parkinson disease: a randomized controlled trial. JAMA284(15), 1931–1938 (2000).
  • McKeith IG, Wesnes KA, Perry E, Ferrara R. Hallucinations predict attentional improvements with rivastigmine in dementia with lewy bodies. Dement. Geriatr. Cogn Disord.18(1), 94–100 (2004).
  • Kaufer DI. Pharmacologic therapy of dementia with Lewy bodies. J. Geriatr. Psychiatry Neurol.15(4), 224–232 (2002).
  • Katz IR, Jeste DV, Mintzer JE, Clyde C, Napolitano J, Brecher M. Comparison of risperidone and placebo for psychosis and behavioral disturbances associated with dementia: a randomized, double-blind trial. Risperidone Study Group. J. Clin. Psychiatry60(2), 107–115 (1999).
  • Walker Z, Grace J, Overshot R et al. Olanzapine in dementia with Lewy bodies: a clinical study. Int. J. Geriatr. Psychiatry14(6), 459–466 (1999).
  • Friedman JH, Fernandez HH. Atypical antipsychotics in Parkinson-sensitive populations. J. Geriatr. Psychiatry Neurol.15(3), 156–170 (2002).
  • Fernandez HH, Trieschmann ME, Burke MA, Friedman JH. Quetiapine for psychosis in Parkinson’s disease versus dementia with Lewy bodies. J. Clin. Psychiatry63(6), 513–515 (2002).
  • Gauthier S, Feldman H, Hecker J et al. Efficacy of donepezil on behavioral symptoms in patients with moderate to severe Alzheimer’s disease. Int. Psychogeriatr.14(4), 389–404 (2002).
  • Wesnes KA, McKeith IG, Ferrara R et al. Effects of rivastigmine on cognitive function in dementia with lewy bodies: a randomised placebo-controlled international study using the cognitive drug research computerised assessment system. Dement. Geriatr. Cogn Disord.13(3), 183–192 (2002).
  • Boeve BF, Silber MH, Ferman TJ. REM Sleep behavior disorder in Parkinson’s disease and dementia with Lewy Bodies. J. Geriatr. Psychiatry Neurol.17(3), 146–157 (2004).
  • Hughes E, Burke RM, Doig AJ. Inhibition of toxicity in the β-amyloid peptide fragment β-25–35 using N-methylated derivatives: a general strategy to prevent amyloid formation. J. Biol. Chem.275(33), 25109–25115 (2000).
  • Alzheimer’s Association. Presented at: The 10th International Conference on Alzheimer’s Disease and Related Disorders. Madrid, Spain, 15–20 July (2006).
  • Lipton SA. The molecular basis of memantine action in Alzheimer’s disease and other neurologic disorders: low-affinity, uncompetitive antagonism. Curr. Alzheimer Res.2(2), 155–165 (2005).
  • Koldamova R Lefterov I. Role of LXR and ABCA1 in the pathogenesis of Alzheimer’s disease - implications for a new therapeutic approach. Curr. Alzheimer Res.4(2), 171–178 (2007).
  • Aisen PS, Schafer KA, Grundman M et al. Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. JAMA289(21), 2819–2826 (2003).
  • Hendrie HC, Hall KS, Ogunniyi A, Gao S. Alzheimer’s disease, genes, and environment: the value of international studies. Can. J. Psychiatr.49(2), 92–99 (2004).
  • Sadowski MJ, Pankiewicz J, Scholtzova H et al. Blocking the apolipoprotein E/amyloid-β interaction as a potential therapeutic approach for Alzheimer’s disease. Proc. Natl Acad. Sci. USA103(49), 18787–18792 (2006).
  • Yao J, Taylor M, Davey F et al. Interaction of amyloid binding alcohol dehydrogenase/Aβ mediates up-regulation of peroxiredoxin II in the brains of Alzheimer’s disease patients and a transgenic Alzheimer’s disease mouse model. Mol. Cell. Neurosci.35(2), 377–382 (2007).
  • Husemann J, Silverstein SC. Expression of scavenger receptor class B, type I, by astrocytes and vascular smooth muscle cells in normal adult mouse and human brain and in Alzheimer’s disease brain. Am. J. Pathol.158(3), 825–832 (2001).
  • Bosco DA, Fowler DM, Zhang Q et al. Elevated levels of oxidized cholesterol metabolites in Lewy body disease brains accelerate α-synuclein fibrilization. Nat. Chem. Biol.2(5), 249–253 (2006).
  • Behl C, Sagara Y. Mechanism of amyloid-β protein induced neuronal cell death: current concepts and future perspectives. J. Neural Trans.49, 125–134 (1997).
  • Tucker JM, Townsend DM. α-tocopherol: roles in prevention and therapy of human disease. Biomed. Pharmacother.59(7), 380–387 (2005).
  • Ono K, Hasegawa K, Naiki H, Yamada M. Preformed β-amyloid fibrils are destabilized by coenzyme Q10 in vitro. Biochem. Biophys. Res. Commun.330(1), 111–116 (2005).
  • Shults CW, Oakes D, Kieburtz K et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch. Neurol.59(10), 1541–1550 (2002).
  • Young AJ, Johnson S, Steffens DC, Doraiswamy PM. Coenzyme Q10: a review of its promise as a neuroprotectant. CNS Spectr.12(1), 62–68 (2007).
  • Espeseth AS, Xu M, Huang Q et al. Compounds that bind APP and inhibit Aβ processing in vitro suggest a novel approach to Alzheimer disease therapeutics. J. Biol. Chem.280(18), 17792–17797 (2005).
  • Kojro E, Fahrenholz F. The non-amyloidogenic pathway: structure and function of α-secretases. Subcell. Biochem.38, 105–127 (2005).
  • Higuchi M, Iwata N, Saido TC. Understanding molecular mechanisms of proteolysis in Alzheimer’s disease: progress toward therapeutic interventions. Biochim. Biophys. Acta1751(1), 60–67 (2005).
  • Huang HC, Klein PS. Multiple roles for glycogen synthase kinase-3 as a drug target in Alzheimer’s disease. Curr. Drug Targets7(11), 1389–1397 (2006).
  • Gilman S, Koller M, Black RS et al. Clinical effects of Aβ immunization (AN1792) in patients with AD in an interrupted trial. Neurology64(9), 1553–1562 (2005).
  • Hock C, Konietzko U, Streffer JR et al. Antibodies against β-amyloid slow cognitive decline in Alzheimer’s disease. Neuron38(4), 547–554 (2003).
  • 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. Psychiatr.75(10), 1472–1474 (2004).
  • Sigurdsson EM, Knudsen E, Asuni A et al. An attenuated immune response is sufficient to enhance cognition in an Alzheimer’s disease mouse model immunized with amyloid-β derivatives. J. Neurosci.24(28), 6277–6282 (2004).
  • Weiner HL, Lemere CA, Maron R et al. Nasal administration of amyloid-β peptide decreases cerebral amyloid burden in a mouse model of Alzheimer’s disease. Ann. Neurol.48(4), 567–579 (2000).
  • Okura Y, Miyakoshi A, Kohyama K, Park IK, Staufenbiel M, Matsumoto Y. Nonviral Aβ DNA vaccine therapy against Alzheimer’s disease: long-term effects and safety. Proc. Natl Acad. Sci. USA103(25), 9619–9624 (2006).
  • Schiltz JG, Salzer U, Mohajeri MH et al. Antibodies from a DNA peptide vaccination decrease the brain amyloid burden in a mouse model of Alzheimer’s disease. J. Mol. Med.82(10), 706–714 (2004).
  • Mruthinti S, Schade RF, Harrell DU et al. Autoimmunity in Alzheimer’s disease as evidenced by plasma immunoreactivity against RAGE and Aβ42: complication of diabetes. Curr. Alzheimer Res.3(3), 229–235 (2006).

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