Development of Parkinson’s disease biomarkers

References

• Biomarkers Definitions Working Group. Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Clin. Pharmacol. Ther.69(3), 89–95 (2001).
   PubMed Web of Science ®Google Scholar
• Hoehn MM, Yahr MD. Parkinsonism: onset, progression and mortality. Neurology17(5), 427–442 (1967).
   PubMed Web of Science ®Google Scholar
• Hughes AJ, Daniel SE, Lees AJ. Improved accuracy of clinical diagnosis of Lewy body Parkinson’s disease. Neurology57(8), 1497–1499 (2001).
   PubMed Web of Science ®Google Scholar
• Perlmutter JS. Assessment of Parkinson disease manifestations. Curr. Protoc. Neurosci. Chapter 10: Unit 10.1 (2009).
   Google Scholar
• Marttila RJ, Rinne UK. Disability and progression in Parkinson’s disease. Acta Neurol. Scand.56(2), 159–169 (1977).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group. Effects of tocopherol and deprenyl on the progression of disability in early Parkinson’s disease. The Parkinson Study Group. N. Engl. J. Med.328(3), 176–183 (1993).
   PubMed Web of Science ®Google Scholar
• Fahn S, Oakes D, Shoulson I et al. Levodopa and the progression of Parkinson’s disease. N. Engl. J. Med.351(24), 2498–2508 (2004).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group. A controlled, randomized, delayed-start study of rasagiline in early Parkinson disease. Arch. Neurol.61(4), 561–566 (2004).
   PubMed Web of Science ®Google Scholar
• Hely MA, Morris JG, Reid WG, Trafficante R. Sydney Multicenter Study of Parkinson’s disease: non-L-dopa-responsive problems dominate at 15 years. Mov. Disord.20(2), 190–199 (2005).
   PubMed Web of Science ®Google Scholar
• Hely MA, Morris JG, Traficante R, Reid WG, O’Sullivan DJ, Williamson PM. The Sydney multicentre study of Parkinson’s disease: progression and mortality at 10 years. J. Neurol. Neurosurg. Psychiatry67(3), 300–307 (1999).
   PubMed Web of Science ®Google Scholar
• Alves G, Wentzel-Larsen T, Aarsland D, Larsen JP. Progression of motor impairment and disability in Parkinson disease: a population-based study. Neurology65(9), 1436–1441 (2005).
   PubMed Web of Science ®Google Scholar
• Sato K, Hatano T, Yamashiro K et al. Prognosis of Parkinson’s disease: time to stage III, IV, V, and to motor fluctuations. Mov. Disord.21(9), 1384–1395 (2006).
   PubMed Web of Science ®Google Scholar
• Jankovic J, Kapadia AS. Functional decline in Parkinson disease. Arch. Neurol.58(10), 1611–1615 (2001).
   PubMedGoogle Scholar
• Louis ED, Tang MX, Cote L, Alfaro B, Mejia H, Marder K. Progression of parkinsonian signs in Parkinson disease. Arch. Neurol.56(3), 334–337 (1999).
   PubMedGoogle Scholar
• Burn DJ, Rowan EN, Allan LM, Molloy S, O’Brien JT, McKeith IG. Motor subtype and cognitive decline in Parkinson’s disease, Parkinson’s disease with dementia, and dementia with Lewy bodies. J. Neurol. Neurosurg. Psychiatry77(5), 585–589 (2006).
   PubMed Web of Science ®Google Scholar
• Goetz CG, Stebbins GT, Blasucci LM. Differential progression of motor impairment in levodopa-treated Parkinson’s disease. Mov. Disord.15(3), 479–484 (2000).
   Google Scholar
• Schrag A, Dodel R, Spottke A, Bornschein B, Siebert U, Quinn NP. Rate of clinical progression in Parkinson‘s disease. A prospective study. Mov. Disord.22(7), 938–945 (2007).
   PubMed Web of Science ®Google Scholar
• Ransmayr G, Kunig G, Neubauer M, Wagner M, Falk M. Effect of age and disease duration on parkinsonian motor scores under levodopa therapy. J. Neural. Transm. Park. Dis. Dement. Sect.9(2–3), 177–188 (1995).
   Google Scholar
• Ross GW, Petrovitch H, Abbott RD et al. Association of olfactory dysfunction with risk for future Parkinson’s disease. Ann. Neurol.63(2), 167–173 (2008).
   PubMed Web of Science ®Google Scholar
• Abbott RD, Petrovitch H, White LR et al. Frequency of bowel movements and the future risk of Parkinson’s disease. Neurology57(3), 456–462 (2001).
   PubMed Web of Science ®Google Scholar
• Iranzo A, Molinuevo JL, Santamaria J et al. Rapid-eye-movement sleep behaviour disorder as an early marker for a neurodegenerative disorder: a descriptive study. Lancet Neurol.5(7), 572–577 (2006).
   PubMed Web of Science ®Google Scholar
• Shiba M, Bower JH, Maraganore DM et al. Anxiety disorders and depressive disorders preceding Parkinson’s disease: a case–control study. Mov. Disord.15(4), 669–677 (2000).
   PubMed Web of Science ®Google Scholar
• Braak H, Del Tredici K, Rüb U, de Vos RA, Jansen Steur EN, Braak E. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol. Aging24(2), 197–211 (2003).
   PubMed Web of Science ®Google Scholar
• Maetzler W, Liepelt I, Berg D. Progression of Parkinson’s disease in the clinical phase: potential markers. Lancet Neurol.8(12), 1158–1171 (2009).
   PubMed Web of Science ®Google Scholar
• Haehner A, Boesveldt S, Berendse HW et al. Prevalence of smell loss in Parkinson’s disease – a multicenter study. Parkinsonism Relat. Disord.15(7), 490–494 (2009).
   PubMedGoogle Scholar
• Herting B, Schulze S, Reichmann H, Haehner A, Hummel T. A longitudinal study of olfactory function in patients with idiopathic Parkinson’s disease. J. Neurol.255(3), 367–370 (2008).
   PubMedGoogle Scholar
• Doty RL, Deems DA, Stellar S. Olfactory dysfunction in parkinsonism: a general deficit unrelated to neurologic signs, disease stage, or disease duration. Neurology38(8), 1237–1244 (1988).
   PubMed Web of Science ®Google Scholar
• Kim JY, Lee WY, Chung EJ, Dhong HJ. Analysis of olfactory function and the depth of olfactory sulcus in patients with Parkinson‘s disease. Mov. Disord.22(11), 1563–1566 (2007).
   Google Scholar
• Verbaan D, Boesveldt S, van Rooden SM et al. Is olfactory impairment in Parkinson disease related to phenotypic or genotypic characteristics? Neurology71(23), 1877–1882 (2008).
   Google Scholar
• Gagnon JF, Postuma RB, Mazza S, Doyon J, Montplaisir J. Rapid-eye-movement sleep behaviour disorder and neurodegenerative diseases. Lancet Neurol.5, 424–432 (2006).
   Web of Science ®Google Scholar
• Boeve BF, Silber MH, Saper CB et al. Pathophysiology of REM sleep behaviour disorder and relevance to neurodegenerative disease. Brain130, 2770–2788 (2007).
   PubMed Web of Science ®Google Scholar
• Schenck CH, Bundlie SR, Mahowald MW. Delayed emergence of a parkinsonian disorder in 38% of 29 older men initially diagnosed with idiopathic rapid eye movement sleep behaviour disorder. Neurology46, 388–393 (1996).
   PubMed Web of Science ®Google Scholar
• Postuma RB, Gagnon JF, Vendette M, Fantini ML, Massicotte-Marquez J, Montplaisir J. Quantifying the risk of neurodegenerative disease in idiopathic REM sleep behavior disorder. Neurology72, 1296–1300 (2009).
   PubMed Web of Science ®Google Scholar
• de Lau LM, Giesbergen PC, de Rijk MC et al. Incidence of parkinsonism and Parkinson disease in a general population: the Rotterdam Study. Neurology63(7), 1240–1244 (2004).
   PubMed Web of Science ®Google Scholar
• Aarsland D, Andersen K, Larsen JP et al. Risk of dementia in Parkinson’s disease: a community-based, prospective study. Neurology56(6), 730–736 (2001).
   PubMed Web of Science ®Google Scholar
• Williams-Gray CH, Foltynie T, Brayne CE et al. Evolution of cognitive dysfunction in an incident Parkinson’s disease cohort. Brain130(7), 1787–1798 (2007).
   PubMed Web of Science ®Google Scholar
• Locascio JJ, Corkin S, Growdon JH. Relation between clinical characteristics of Parkinson’s disease and cognitive decline. J. Clin. Exp. Neuropsychol.25(1), 94–109 (2003).
   PubMed Web of Science ®Google Scholar
• Muslimovic D, Post B, Speelman JD et al. Cognitive decline in Parkinson’s disease: a prospective longitudinal study. J. Int. Neuropsychol. Soc.15(3), 426–437 (2009).
   PubMed Web of Science ®Google Scholar
• Janvin CC, Larsen JP, Aarsland D et al. Subtypes of mild cognitive impairment in Parkinson’s disease: progression to dementia. Mov. Disord.21(9), 1343–1349 (2006).
   PubMed Web of Science ®Google Scholar
• Muslimovic D, Post B, Speelman JD et al. Cognitive profile of patients with newly diagnosed Parkinson disease. Neurology65(8), 1239–1245 (2005).
   PubMed Web of Science ®Google Scholar
• Caviness JN, Driver-Dunckley E, Connor DJ et al. Defining mild cognitive impairment in Parkinson’s disease. Mov. Disord.22(9), 1272–1277 (2007).
   PubMed Web of Science ®Google Scholar
• Williams-Gray CH, Evans JR, Goris A et al. The distinct cognitive syndromes of Parkinson’s disease: 5 year follow-up of the CamPaIGN cohort. Brain132(Pt 11), 2958–2969 (2009).
   PubMed Web of Science ®Google Scholar
• Factor SA, Feustel PJ, Friedman JH et al. Longitudinal outcome of Parkinson’s disease patients with psychosis. Neurology60(11), 1756–1761 (2003)
   PubMed Web of Science ®Google Scholar
• Goetz CG, Stebbins GT. Risk factors for nursing home placement in advanced Parkinson’s disease. Neurology43(11), 2227–2229 (1993).
   PubMed Web of Science ®Google Scholar
• Goetz CG, Stebbins GT. Mortality and hallucinations in nursing home patients with advanced Parkinson’s disease. Neurology45(4), 669–671 (1995).
   PubMed Web of Science ®Google Scholar
• Aarsland D, Larsen JP, Cummins JL, Laake K. Prevalence and clinical correlates of psychotic symptoms in Parkinson disease: a community-based study. Arch. Neurol.56(5), 595–601 (1999).
   PubMed Web of Science ®Google Scholar
• Aarsland D, Zaccai J, Brayne C. A systematic review of prevalence studies of dementia in Parkinson’s disease. Mov. Disord.20(10), 1255–1263 (2005).
   PubMed Web of Science ®Google Scholar
• 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).
   PubMed Web of Science ®Google Scholar
• Hely MA, Reid WG, Adena MA, Halliday GM, Morris JG. The Sydney multicenter study of Parkinson’s disease: the inevitability of dementia at 20 years. Mov. Disord.23(6), 837–844 (2008).
   PubMed Web of Science ®Google Scholar
• Williams-Gray CH, Foltynie T, Brayne CE, Robbins TW, Barker RA. Evolution of cognitive dysfunction in an incident Parkinson’s disease cohort. Brain130(7), 1787–1798 (2007).
   PubMed Web of Science ®Google Scholar
• Jakowec MW, Petzinger GM, Sastry S, Donaldson DM, McCormack A, Langston JW. The native form of α-synuclein is not found in the cerebrospinal fluid of patients with Parkinson’s disease or normal controls. Neurosci. Lett.253(1), 13–16 (1998).
   Google Scholar
• Borghi R, Marchese R, Negro A et al. Full length α-synuclein is present in cerebrospinal fluid from Parkinson’s disease and normal subjects. Neurosci. Lett.287(1), 65–67 (2000).
   PubMed Web of Science ®Google Scholar
• El-Agnaf OM, Salem SA, Paleologou KE et al. Detection of oligomeric forms of α-synuclein protein in human plasma as a potential biomarker for Parkinson’s disease. FASEB J.20(3), 419–425 (2006).
   PubMed Web of Science ®Google Scholar
• Lee PH, Lee G, Park HJ, Bang OY, Joo IS, Huh K. The plasma α-synuclein levels in patients with Parkinson’s disease and multiple system atrophy. J. Neural. Transm.113(10), 1435–1439 (2006).
   PubMed Web of Science ®Google Scholar
• Tokuda T, Salem SA, Allsop D et al. Decreased α-synuclein in cerebrospinal fluid of aged individuals and subjects with Parkinson’s disease. Biochem. Biophys. Res. Commun.349(1), 162–166 (2006).
   PubMed Web of Science ®Google Scholar
• Maita C, Tsuji S, Yabe I et al. Secretion of DJ-1 into the serum of patients with Parkinson’s disease. Neurosci. Lett.431(1), 86–89 (2008).
   Web of Science ®Google Scholar
• Waragai M, Nakai M, Wei J et al. Plasma levels of DJ-1 as a possible marker for progression of sporadic Parkinson‘s disease. Neurosci. Lett.425(1), 18–22 (2007).
   PubMed Web of Science ®Google Scholar
• Hong Z, Shi M, Chung KA, Quinn JF et al. DJ-1 and α-synuclein in human cerebrospinal fluid as biomarkers of Parkinson’s disease. Brain133(Pt 3), 713–726 (2010).
   PubMed Web of Science ®Google Scholar
• Connolly J, Siderowf A, Clark CM, Mu D, Pratico D. F2 isoprostane levels in plasma and urine do not support increased lipid peroxidation in cognitively impaired Parkinson disease patients. Cogn. Behav. Neurol.21(2), 83–86 (2008).
   Google Scholar
• Bogdanov M, Matson WR, Wang L et al. Metabolomic profiling to develop blood biomarkers for Parkinson’s disease. Brain131(2), 389–396 (2008).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group DATATOP Investigators. Urate as a predictor of the rate of clinical decline in Parkinson disease. Arch. Neurol.66(12), 1460–1468 (2009).
   PubMed Web of Science ®Google Scholar
• Zhang J, Sokal I, Peskind ER et al. CSF multianalyte profile distinguishes Alzheimer and Parkinson diseases. Am. J. Clin. Pathol.129(4), 526–529 (2008).
   PubMed Web of Science ®Google Scholar
• Snow BJ, Tooyama I, McGeer EG et al. Human positron emission tomographic 18F-dopa studies correlate with dopamine cell counts and levels. Ann. Neurol.34(3), 324–330 (1993).
   PubMed Web of Science ®Google Scholar
• Pate BD, Kawamata T, Yamada T et al. Correlation of striatal fluorodopa uptake in the MPTP monkey with dopaminergic indices. Ann. Neurol.34(3), 331–338 (1993).
   PubMed Web of Science ®Google Scholar
• Ribeiro MJ, Vidailhet M, Nguyen JP et al. Dopaminergic function and dopamine transporter binding assessed with positron emission tomography in Parkinson disease. Arch. Neurol.59(4), 580–586 (2002).
   PubMedGoogle Scholar
• Brooks DJ, Salmon EP, Mathias CJ et al. The relationship between locomotor disability, autonomic dysfunction, and the integrity of the striatal dopaminergic system in patients with multiple system atrophy, pure autonomic failure and Parkinson’s disease studied by PET. Brain113(5), 1539–1552 (1990).
   Google Scholar
• Vingerhoets FJG, Schulzer M, Calne DB, Snow BJ. Which clinical sign of Parkinson’s disease best reflects the nigrostriatal lesion? Ann. Neurol.41(1), 58–64 (1997).
   PubMed Web of Science ®Google Scholar
• Broussolle E, Dentresangle C, Landais P et al. The relation of putamen and caudate nucleus 18F-dopa uptake to motor and cognitive performances in Parkinson’s disease. J. Neurol. Sci.166(2), 141–151 (1999).
   Google Scholar
• Morrish PK, Sawle GV, Brooks DJ. Clinical and [18F] dopa PET findings in early Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry59(6), 597–600 (1995).
   PubMed Web of Science ®Google Scholar
• Kish SJ, Shannak K, Hornykiewicz O. Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. Pathophysiologic and clinical implications. N. Engl. J. Med.318(14), 876–880 (1988).
   PubMed Web of Science ®Google Scholar
• Rakshi JS, Uema T, Ito K et al. Frontal, midbrain and striatal dopaminergic function in early and advanced Parkinson’s disease. A 3D [18F]Dopa-PET study. Brain122(9), 1637–1650 (1999).
   PubMed Web of Science ®Google Scholar
• Kaasinen V, Nurmi E, Brück A et al. Increased frontal [(18)F]fluorodopa uptake in early Parkinson’s disease: sex differences in the prefrontal cortex. Brain124(6), 1125–1130 (2001).
   PubMed Web of Science ®Google Scholar
• Whone AL, Moore RY, Piccini P, Brooks DJ. Plasticity of the nigropallidal pathway in Parkinson’s disease. Ann. Neurol.53(2), 206–213 (2003).
   PubMed Web of Science ®Google Scholar
• Seibyl JP, Marek KL, Quinlan D et al. Decreased singlephoton emission computed tomographic [123I]β-CIT striatal uptake correlates with symptom severity in Parkinson’s disease. Ann. Neurol.38(4), 589–598 (1995).
   PubMed Web of Science ®Google Scholar
• Brucke T, Asenbaum S, Pirker W et al. Measurement of dopaminergic degeneration in Parkinson’s disease with [123I]β-CIT and SPECT. Correlation with clinical findings and comparison with multiple system atrophy and progressive supranuclear palsy. J. Neural. Transm.50, 9–24 (1997).
   Google Scholar
• Pirker W. Correlation of dopamine transporter imaging with parkinsonian motor handicap: how close is it? Mov. Disord.18(Suppl. 7), S43–S51 (2003).
   Google Scholar
• Pirker W, Asenbaum S, Hauk M et al. Imaging serotonin and dopamine transporters with 123I-β-CIT SPECT: binding kinetics and effects of normal aging. J. Nucl. Med.41(1), 36–44 (2000).
   PubMed Web of Science ®Google Scholar
• van Dyck CH, Seibyl JP, Malison RT et al. Age-related decline in striatal dopamine transporter binding with iodine-123-β-CITSPECT. J. Nucl. Med.36(7), 1175–1181 (1995).
   PubMed Web of Science ®Google Scholar
• Liu Y, Edwards RH. The role of the vescicular transport proteins in the synaptic transmission and neural degeneration. Annu. Rev. Neurosci.20, 125–156 (1997).
   PubMed Web of Science ®Google Scholar
• Lee CS, Samii A, Sossi V et al.In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopamine nerve terminals in Parkinson’s disease. Ann. Neurol.47(4), 493–503 (2000).
   PubMed Web of Science ®Google Scholar
• Ouchi Y, Yoshikawa E, Sekine Y et al. Microglial activation and dopamine terminal loss in early Parkinson’s disease. Ann. Neurol.57(2), 168–175 (2005).
   PubMed Web of Science ®Google Scholar
• Gerhard A, Pavese N, Hotton G et al.In vivo imaging of microglial activation with [11C](R)- PK11195 PET in idiopathic Parkinson’s disease. Neurobiol. Dis.21(2), 404–412 (2006).
   PubMed Web of Science ®Google Scholar
• Eshuis SA, Jager PL, Maguire RP, Jonkman S, Dierckx RA, Leenders KL. Direct comparison of FP-CIT SPECT and F-DOPA PET in patients with Parkinson’s disease and healthy controls. Eur. J. Nucl. Med. Mol. Imaging36(3), 454–462 (2009).
   Google Scholar
• Piccini P, Burn DJ, Ceravolo R, Maraganore D, Brooks DJ. The role of inheritance in sporadic Parkinson’s disease: evidence from a longitudinal study of dopaminergic function in twins. Ann. Neurol.45(5), 577–582 (1999).
   PubMed Web of Science ®Google Scholar
• Piccini P, Morrish PK, Turjanski N et al. Dopaminergic function in familial Parkinson’s disease: a clinical and 18F-dopa PET study. Ann. Neurol.41(2), 222–229 (1997).
   Google Scholar
• Hilker R, Klein C, Hedrich K et al. The striatal dopaminergic deficit is dependent on the number of mutant alleles in a family with mutations in the parkin gene: evidence for enzymatic parkin function in humans. Neurosci. Lett.323(1), 50–54 (2002).
   Google Scholar
• Khan NL, Scherfler C, Graham E et al. Dopaminergic dysfunction in unrelated, asymptomatic carriers of a single parkin mutation. Neurology64(1), 134–136 (2005).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group-PROGENI Investigators. Parkin dosage mutations have greater pathogenicity in familial PD than simple sequence mutations. Neurology73(4), 279–286 (2009).
   PubMed Web of Science ®Google Scholar
• Schwingenschuh P, Ruge D, Edwards MJ et al. Distinguishing SWEDDs patients with asymmetric resting tremor from Parkinson’s disease: a clinical and electrophysiological study. Mov. Disord.25(5), 560–569 (2010).
   PubMed Web of Science ®Google Scholar
• Ponsen MM, Stoffers D, Wolters ECH, Booij J, Berendse HW. Olfactory testing combined with dopamine transporter imaging as a method to detect prodromal Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry81(4), 396–399 (2010).
   PubMed Web of Science ®Google Scholar
• Morrish PK, Rakshi JS, Bailey DL, Sawle G, Brooks DJ. Measuring the rate of progression and estimating the preclinical period of Parkinson’s disease with 18F-dopa PET. J. Neurol. Neurosurg. Psychiatry64(3), 314–319 (1998).
   PubMed Web of Science ®Google Scholar
• Nurmi E, Ruottinen HM, Bergman J et al. Rate of progression in Parkinson’s disease: a 18-F-fluoro-dopa PET study. Mov. Disord.16(4), 608–615 (2001).
   PubMed Web of Science ®Google Scholar
• Brück A, Aalto S, Nurmi E, Vahlberg T, Bergman J, Rinne JO. Striatal subregional 6-[18F] fluoro-L-dopa uptake in early Parkinson’s disease: a two-year follow-up study. Mov. Disord.21(7), 958–963 (2006).
   PubMedGoogle Scholar
• Marek K, Innis R, van Dyck C et al. [123I] β-CIT SPECT imaging assessment of the rate of Parkinson’s disease progression. Neurology57(11), 2089–2094 (2001).
   PubMed Web of Science ®Google Scholar
• Pirker W, Djamshidian S, Asenbaum S et al. Progression of dopaminergic degeneration in Parkinson’s disease and atypical parkinsonism: a longitudinal β-CIT SPECT study. Mov. Disord.17(1), 45–53 (2002).
   PubMed Web of Science ®Google Scholar
• Winogrodzka A, Bergmans P, Booij J, van Royen EA, Stoof JC, Wolters EC. [(123)I] β-CIT SPECT is a useful method for monitoring dopaminergic degeneration in early stage Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry74(3), 294–298 (2003).
   PubMed Web of Science ®Google Scholar
• Tang CC, Poston KL, Dhawan V, Eidelberg D. Abnormalities in metabolic network activity precede the onset of motor symptoms in Parkinson’s disease. J. Neurosci.30(3), 1049–1056 (2010).
   PubMed Web of Science ®Google Scholar
• Nandhagopal R, Kuramoto L, Schulzer M et al. Longitudinal progression of sporadic Parkinson‘s disease: a multi-tracer positron emission tomography study. Brain132(11), 2970–2979 (2009)
   PubMed Web of Science ®Google Scholar
• Sossi V, de la Fuente-Fernández R, Holden JE, Schulzer M, Ruth TJ, Stoessl J. Changes of dopamine turnover in the progression of Parkinson’s disease as measured by positron emission tomography: their relation to disease-compensatory mechanisms. J. Cereb. Blood Flow Metab.24(8), 869–876 (2004).
   PubMed Web of Science ®Google Scholar
• Rascol O, Brooks DJ, Korczyn AD et al. A five-year study of the incidence of dyskinesia in patients with early Parkinson’s disease who were treated with ropinirole or levodopa. (056 study group). N. Engl. J. Med.342(20), 1484–1491 (2000).
   PubMed Web of Science ®Google Scholar
• Clarke CE, Guttman M. Dopamine agonist monotherapy in Parkinson’s disease. Lancet360(9347), 1767–1769 (2002).
   PubMed Web of Science ®Google Scholar
• Rakshi JS, Pavese N, Uema T et al. A comparison of the progression of early Parkinson’s disease in patients started on ropinirole or L-dopa: an 18F-dopa PET study. J. Neural Transm.109(12), 1433–1443 (2002).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group. Dopamine transporter brain imaging to assess the effects of pramipexole vs levodopa on Parkinson disease progression. JAMA287(13), 1653–1661 (2002).
   PubMed Web of Science ®Google Scholar
• Whone AL, Watts RL, Stoessl AJ et al. Slower progression of Parkinson’s disease with ropinirole versus levodopa: the REAL-PET study. Ann. Neurol.54(1), 93–101 (2003).
   PubMed Web of Science ®Google Scholar
• Fahn S, Oakes D, Shoulson I et al. Levodopa and the progression of Parkinson’s disease. N. Engl. J. Med.351(24), 2498–2508 (2004).
   PubMed Web of Science ®Google Scholar
• Gill SS, Patel NK, Hotton GR et al. Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease. Nat. Med.9(5), 589–595 (2003).
   PubMed Web of Science ®Google Scholar
• Brundin P, Pogarell O, Hagell P et al. Bilateral caudate and putamen grafts of embryonic mesencephalic tissue treated with lazaroids in Parkinson’s disease. Brain123(7), 1380–1390 (2000).
   PubMed Web of Science ®Google Scholar
• Hornykiewicz O. Biochemical aspects of Parkinson’s disease. Neurology51(Suppl. 2), S2–S9 (1998).
   PubMed Web of Science ®Google Scholar
• Moore RY, Whone AL, Brooks DJ. Extrastriatal monoamine neuron function in Parkinson’s disease: an 18F-dopa PET study. Neurobiol. Dis.29(3), 381–390 (2008).
   Google Scholar
• Seibyl JP, Wallace E, Smith EO et al. Whole-body biodistribution, radiation absorbed dose, and brain SPECT imaging with iodine-123-β-CIT in healthy human subjects. J. Nucl. Med.35(5), 764–770 (1994).
   Google Scholar
• Kim SE, Choi JY, Choe YS, Choi Y, Lee Y. Serotonin transporters in the midbrain of Parkinson’s disease patients: a study with 123I-β-CIT SPECT. J. Nucl. Med.44(6), 870–876 (2003).
   Google Scholar
• Brooks DJ, Piccini P. Imaging in Parkinson’s disease: the role of monoaminesin behavior. Biol. Psychiatry59(10), 908–918 (2006).
   Google Scholar
• Guttman M, Boileau I, Warsh J et al. Brain serotonin transporter binding in non-depressed patients with Parkinson’s disease. Eur. J. Neurol.14(5), 523–528 (2007).
   PubMedGoogle Scholar
• Doder M, Rabiner EA, Turjanski N, Lees AJ, Brooks DJ. Tremor in Parkinson’s disease and serotonergic dysfunction: an 11C-WAY 100635 PET study. Neurology60(4), 601–605 (2003).
   PubMedGoogle Scholar
• Remy P, Doder M, Lees AJ, Turjanski N, Brooks DJ. Depression in Parkinson’s disease: loss of dopamine and noradrenaline innervation in the limbic system. Brain128(6), 1314–1322 (2005).
   PubMed Web of Science ®Google Scholar
• Kuhl DE, Minoshima S, Fessler JA et al. In vivo mapping of cholinergic terminals in normal aging, Alzheimer’s disease and Parkinson’s disease. Ann. Neurol.40(3), 399–410 (1996).
   PubMed Web of Science ®Google Scholar
• Hilker R, Thomas AV, Klein JC et al. Dementia in Parkinson disease: functional imaging of cholinergic and dopaminergic pathways. Neurology65(11), 1716–1722 (2005).
   PubMed Web of Science ®Google Scholar
• Schrag A, Good CD, Miszkiel K et al. Differentiation of atypical parkinsonian syndromes with routine MRI. Neurology54(3), 697–702 (2000).
   PubMed Web of Science ®Google Scholar
• Dexter DT, Wells FR, Agid F et al. Increased nigral iron content in postmortem parkinsonian brain. Lancet2(8569), 1219–1220 (1987).
   PubMed Web of Science ®Google Scholar
• Antonini A, Leenders KL, Meier D, Oertel WH, Boesiger P, Anliker M. T2 relaxation time in patients with Parkinson’s disease. Neurology43(4), 697–700 (1993).
   Google Scholar
• Vymazal J, Righini A, Brooks RA et al. T1 and T2 in the brain of healthy subjects, patients with Parkinson disease, and patients with multiple system atrophy: relation to iron content. Radiology211(2), 489–495 (1999).
   Google Scholar
• Hutchinson M, Raff U. Structural changes of the substantia nigra in Parkinson’s disease as revealed by MR imaging. Am. J. Neuroradiol.21(4), 697–701 (2000).
   PubMed Web of Science ®Google Scholar
• Hu MT, White SJ, Herlihy AH, Chaudhuri KR, Hajnal JV, Brooks DJ. A comparison of (18)F-dopa PET and inversion recovery MRI in the diagnosis of Parkinson’s disease. Neurology56(9), 1195–1200 (2001).
   PubMedGoogle Scholar
• Martin WR. Quantitative estimation of regional brain iron with magnetic resonance imaging. Parkinsonism Relat. Disord.15(Suppl. 3), S215–S218 (2009).
   Google Scholar
• Martin WR, Wieler M, Gee M. Midbrain iron content in early Parkinson disease: a potential biomarker of disease status. Neurology70(16), 1411–1417 (2008).
   PubMed Web of Science ®Google Scholar
• Ashburner J, Friston KJ. Voxel-based morphometry – the methods. NeuroImage11(6), 805–821 (2000).
   PubMed Web of Science ®Google Scholar
• Burton EJ, McKeith IG, Burn DJ, Williams ED, O’Brien JT. Cerebral atrophy in Parkinson’s disease with and without dementia: a comparison with Alzheimer’s disease, dementia with Lewy bodies and controls. Brain127(4), 791–800 (2004).
   PubMed Web of Science ®Google Scholar
• Summerfield C, Junqué C, Tolosa E et al. Structural brain changes in Parkinson disease with dementia: a voxel-based morphometry study. Arch. Neurol.62(2), 281–285 (2005).
   PubMedGoogle Scholar
• Ibarretxe-Bilbao N, Ramirez-Ruiz B, Junque C et al. Differential progression of brain atrophy in Parkinson disease with and without visual hallucinations. J. Neurol. Neurosurg. Psychiatry.81(6), 650–657 (2010).
   PubMed Web of Science ®Google Scholar
• Ibarretxe-Bilbao N, Tolosa E, Junque C, Marti MJ. MRI and cognitive impairment in Parkinson’s disease. Mov. Disord.24(Suppl. 2), S748–S753 (2009).
   Google Scholar
• Beyer MK, Janvin CC, Larsen JP, Aarsland D. A magnetic resonance imaging study of patients with Parkinson’s disease with mild cognitive impairment and dementia using voxel-based morphometry. J. Neurol. Neurosurg. Psychiatry78(3), 254–259 (2007).
   PubMed Web of Science ®Google Scholar
• Feldmann A, Illes Z, Kosztolanyi P et al. Morphometric changes of gray matter in Parkinson’s disease with depression: a voxel-based morphometry study. Mov. Disord.23(1), 42–46 (2008).
   Google Scholar
• Yoshikawa K, Nakata Y, Yamada K, Nakagawa M. Early pathological changes in the parkinsonian brain demonstrated by diffusion tensor MRI. J. Neurol. Neurosurg. Psychiatry75(3), 481–484 (2004).
   PubMed Web of Science ®Google Scholar
• Chan LL, Rumpel H, Yap K et al. Case control study of diffusion tensor imaging in Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry78(12), 1383–1386 (2007).
   PubMedGoogle Scholar
• Scherfler C, Schocke MF, Seppi K et al. Voxel-wise analysis of diffusion weighted imaging reveals disruption of the olfactory tract in Parkinson’s disease. Brain129(2), 538–542 (2006).
   PubMed Web of Science ®Google Scholar
• Matsui H, Nishinaka K, Oda M et al. Depression in Parkinson’s disease. Diffusion tensor imaging study. J. Neurol.254(9), 1170–1173 (2007).
   Google Scholar
• Matsui H, Nishinaka K, Oda M, Niikawa H, Kubori T, Udaka F. Dementia in Parkinson’s disease: diffusion tensor imaging. Acta Neurol. Scand.116(3), 177–181 (2007).
   Google Scholar
• Berg D. Transcranial ultrasound as a risk marker for Parkinson’s disease. Mov. Disord.24(Suppl. 2), S677–S683 (2009).
   Google Scholar
• Berg D, Godau J, Walter U. Transcranial sonography in movement disorders. Lancet Neurol.7(11), 1044–1055 (2008).
   PubMed Web of Science ®Google Scholar
• Berg D, Merz B, Reiners K, Naumann M, Becker G. Five-year follow-up study of hyperechogenicity of the substantia nigra in Parkinson’s disease. Mov. Disord.20(3), 383–385 (2005).
   PubMed Web of Science ®Google Scholar
• Berg D, Becker G, Zeiler B et al. Vulnerability of the nigrostriatal system as detected by transcranial ultrasound. Neurology53(5), 1026–1031 (1999).
   PubMed Web of Science ®Google Scholar
• Hoeppner J, Prudente-Morrissey L, Herpertz SC, Benecke R, Walter U. Substantia nigra hyperechogenicity in depressive subjects relates to motor asymmetry and impaired word fluency. Eur. Arch. Psychiatry Clin. Neurosci.259(2), 92–97 (2009).
   PubMed Web of Science ®Google Scholar
• Walter U, Dressler D, Probst T et al. Transcranial brain sonography findings in discriminating between parkinsonism and idiopathic Parkinson disease. Arch. Neurol.64(11), 1635–1640 (2007).
   PubMedGoogle Scholar
• Walter U, Dressler D, Wolters A, Probst T, Grossmann A, Benecke R. Sonographic discrimination of corticobasal degeneration vs progressive supranuclear palsy. Neurology63(3), 504–509 (2004).
   PubMed Web of Science ®Google Scholar
• Stockner H, Sojer M, K KS et al. Midbrain sonography in patients with essential tremor. Mov. Disord.22(3), 414–417 (2007).
   PubMed Web of Science ®Google Scholar
• Berg D, Siefker C, Ruprecht-Dorfler P, Becker G. Relationship of substantia nigra echogenicity and motor function in elderly subjects. Neurology56(1), 13–17 (2001).
   PubMedGoogle Scholar
• Courbon F, Brefel-Courbon C, Thalamas C, Alibelli MJ, Berry I, Montastruc JL. Cardiac MIBG scintigraphy is a sensitive tool for detecting cardiac sympathetic denervation in Parkinson’s disease. Mov. Disord.18(8), 890–897 (2003).
   PubMed Web of Science ®Google Scholar
• Ishibashi K, Saito Y, Murayama S et al. Validation of cardiac (123)I-MIBG scintigraphy in patients with Parkinson’s disease who were diagnosed with dopamine PET. Eur. J. Nucl. Med. Mol. Imaging37(1), 3–11 (2010).
   Google Scholar
• Fröhlich I, Diederich NJ, Pilloy W, Vaillant M. Myocardial MIBG scintigraphy: a useful clinical tool?: a retrospective study in 50 parkinsonian patients. Neurol. Sci.31(3), 403–406 (2010).
   Web of Science ®Google Scholar
• Tan EK, Skipper L. Pathogenic mutations in Parkinson’s disease. Hum Mutat.28(7), 641–653 (2007).
   PubMedGoogle Scholar
• Tan EK. The role of common genetic risk variants in Parkinson disease. Clin. Genet.72(5), 387–393 (2007).
   Google Scholar
• Goldberg MS, Lansbury PT Jr. Is there a cause-and-effect relationship between α-synuclein fibrillization and Parkinson’s disease? Nat. Cell Biol.2(7), E115–E119 (2000).
   PubMedGoogle Scholar
• Krüger R, Kuhn W, Müller T et al. Ala30Pro mutation in the gene encoding α-synuclein in Parkinson’s disease. Nat. Genet.18(2), 106–108 (1998).
   PubMed Web of Science ®Google Scholar
• Papadimitriou A, Veletza V, Hadjigeorgiou GM, Patrikiou A, Hirano M, Anastasopoulos I. Mutated α-synuclein gene in two Greek kindreds with familial PD: incomplete penetrance? Neurology52(3), 651–654 (1999).
   Google Scholar
• Polymeropoulos MH, Lavedan C, Leroy E et al. Mutation in the α-synuclein gene identified in families with Parkinson’s disease. Science276(5321), 2045–2047 (1997).
   PubMed Web of Science ®Google Scholar
• Singleton AB, Farrer M, Johnson J et al. α-synuclein locus triplication causes Parkinson’s disease. Science302(5646), 841 (2003).
   PubMed Web of Science ®Google Scholar
• Tan EK, Chai A, Teo YY et al. α-synuclein haplotypes implicated in risk of Parkinson’s disease. Neurology62(1), 128–131 (2004).
   PubMed Web of Science ®Google Scholar
• Xiromerisiou G, Hadjigeorgiou GM, Gourbali V et al. Screening for SNCA and LRRK2 mutations in Greek sporadic and autosomal dominant Parkinson’s disease: identification of two novel LRRK2 variants. Eur. J. Neurol.14(1), 7–11 (2007).
   Google Scholar
• Zarranz JJ, Alegre J, Gómez-Esteban JC et al. The new mutation, E46K, of α-synuclein causes Parkinson and Lewy body dementia. Ann. Neurol.55(2), 164–173 (2004).
   PubMed Web of Science ®Google Scholar
• Chartier-Harlin MC, Kachergus J, Roumier C et al. α-synuclein locus duplication as a cause of familial Parkinson’s disease. Lancet364(9440), 1167–1169 (2004).
   PubMed Web of Science ®Google Scholar
• Fuchs J, Nilsson C, Kachergus J et al. Phenotypic variation in a large Swedish pedigree due to SNCA duplication and triplication. Neurology68(12), 916–922 (2007).
   PubMed Web of Science ®Google Scholar
• Eriksen JL, Przedborski S, Petrucelli L. Gene dosage and pathogenesis of Parkinson’s disease. Trends Mol. Med.11(3), 91–96 (2005).
   PubMed Web of Science ®Google Scholar
• Volles MJ, Lansbury PT Jr. Zeroing in on the pathogenic form of α-synuclein and its mechanism of neurotoxicity in Parkinson’s disease. Biochemistry42(26), 7871–7878 (2003).
   PubMed Web of Science ®Google Scholar
• Winkler S, Hagenah J, Lincoln S et al. α-synuclein and Parkinson disease susceptibility. Neurology69(18), 1745–1750 (2007).
   PubMed Web of Science ®Google Scholar
• Cuervo AM, Stefanis L, Fredenburg R, Lansbury PT, Sulzer D. Impaired degradation of mutant α-synuclein by chaperone-mediated autophagy. Science305(5688), 1292–1295 (2004).
   PubMed Web of Science ®Google Scholar
• Massey AC, Kaushik S, Sovak G, Kiffin R, Cuervo AM. Consequences of the selective blockage of chaperone-mediated autophagy. Proc. Natl Acad. Sci. USA103(15), 5805–5810 (2006).
   PubMed Web of Science ®Google Scholar
• Abbas N, Lücking CB, Ricard S et al. A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe. Hum. Mol. Genet.8(4), 567–574 (1999).
   PubMed Web of Science ®Google Scholar
• Betarbet R, Sherer TB, Greenamyre JT. Ubiquitin-proteasome system and Parkinson’s diseases. Exp. Neurol.191(Suppl. 1), S17–S27 (2005).
   PubMed Web of Science ®Google Scholar
• Hasegawa T, Treis A, Patenge N, Fiesel FC, Springer W, Kahle PJ. Parkin protects against tyrosinase-mediated dopamine neurotoxicity by suppressing stress-activated protein kinase pathways. J. Neurochem.105(5), 1700–1715 (2008).
   PubMed Web of Science ®Google Scholar
• Kitada T, Asakawa S, Hattori N et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature392(6676), 605–608 (1998).
   PubMed Web of Science ®Google Scholar
• van de Warrenburg BP, Lammens M, Lücking CB et al. Clinical and pathologic abnormalities in a family with parkinsonism and parkin gene mutations. Neurology56(4), 555–557 (2001).
   PubMed Web of Science ®Google Scholar
• Portman AT, Giladi N, Leenders KL et al. The nigrostriatal dopaminergic system in familial early onset parkinsonism with parkin mutations. Neurology56(12), 1759–1762 (2001).
   Google Scholar
• 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).
   PubMed Web of Science ®Google Scholar
• Tan EK, Refai FS, Siddique M et al. Clinically reported heterozygous mutations in the PINK1 kinase domain exert a gene dosage effect. Hum. Mutat.30(11), 1551–1557 (2009).
   Google Scholar
• Abou-Sleiman PM, Muqit MM, Wood NW. Expanding insights of mitochondrial dysfunction in Parkinson’s disease. Nat. Rev. Neurosci.7(3), 207–219 (2006).
   PubMed Web of Science ®Google Scholar
• Tan EK. PINK1 mutations and differential effects on mitochondrial function. Exp. Neurol.221(1), 10–12 (2010).
   Google Scholar
• Albanese A, Valente EM, Romito LM, Bellacchio E, Elia AE, Dallapiccola B. The PINK1 phenotype can be indistinguishable from idiopathic Parkinson disease. Neurology64(11), 1958–1960 (2005).
   Google Scholar
• Ephraty L, Porat O, Israeli D et al. Neuropsychiatric and cognitive features in autosomalrecessive early parkinsonism due to PINK1 mutations. Mov. Disord.22(4), 566–569 (2007).
   Google Scholar
• Bonifati V, Rizzu P, van Baren MJ et al. Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism. Science299(5604), 256–259 (2003).
   PubMed Web of Science ®Google Scholar
• Canet-Avilés RM, Wilson MA, Miller DW et al. The Parkinson’s disease protein DJ-1 is neuroprotective due to cysteine-sulfinic aciddriven mitochondrial localization. Proc. Natl Acad. Sci. USA101(24), 9103–9108 (2004).
   PubMed Web of Science ®Google Scholar
• Zhang L, Shimoji M, Thomas B et al. Mitochondrial localization of the Parkinson’s disease related protein DJ-1: implications for pathogenesis. Hum. Mol. Genet.14(14), 2063–2073 (2005).
   PubMed Web of Science ®Google Scholar
• Zimprich A, Biskup S, Leitner P et al. Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron44(4), 601–607 (2004).
   PubMed Web of Science ®Google Scholar
• Kumari U, Tan EK. LRRK2 in Parkinson’s disease: genetic and clinical studies from patients. FEBS J.276(22), 6455–6463 (2009).
   PubMed Web of Science ®Google Scholar
• Skipper L, Shen H, Chua E, et al. Analysis of LRRK2 functional domains in nondominant Parkinson disease. Neurology65(8), 1319–1321 (2005).
   Google Scholar
• Healy DG, Falchi M, O’Sullivan SS et al. Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinson’s disease: a case–control study. Lancet Neurol.7(7), 583–590 (2008).
   PubMed Web of Science ®Google Scholar
• Gilks WP, Abou-Sleiman PM, Gandhi S et al. A common LRRK2 mutation in idiopathic Parkinson’s disease. Lancet365(9457), 415–416 (2005).
   PubMed Web of Science ®Google Scholar
• Lesage S, Janin S, Lohmann E et al. LRRK2 exon 41 mutations in sporadic Parkinson disease in Europeans. Arch. Neurol.64(3), 425–430 (2007).
   Google Scholar
• Ozelius LJ, Senthil G, Saunders-Pullman R et al. LRRK2 G2019S as a cause of Parkinson’s disease in Ashkenazi Jews. N. Engl. J. Med.354(4), 424–425 (2006).
   PubMed Web of Science ®Google Scholar
• Tan EK, Zhao Y, Skipper L et al. The LRRK2 Gly2385Arg variant is associated with Parkinson’s disease: genetic and functional evidence. Hum. Genet.120(6), 857–863 (2007).
   Google Scholar
• Lesage S, Dürr A, Tazir M et al. LRRK2 G2019S as a cause of Parkinson’s disease in North African Arabs. N. Engl. J. Med.354(4), 422–423 (2006).
   PubMed Web of Science ®Google Scholar
• Mata IF, Wedemeyer WJ, Farrer MJ, Taylor JP, Gallo KA. LRRK2 in Parkinson’s disease: protein domains and functional insights. Trends Neurosci.29(5), 286–293 (2006).
   PubMed Web of Science ®Google Scholar
• Lu YW, Tan EK. Molecular biology changes associated with LRRK2 mutations in Parkinson’s disease. J. Neurosci. Res.86(9), 1895–1901 (2008).
   PubMed Web of Science ®Google Scholar
• Greggio E, Jain S, Kingsbury A et al. Kinase activity is required for the toxic effects of mutant LRRK2/dardarin. Neurobiol. Dis.23(2), 329–341 (2006).
   PubMed Web of Science ®Google Scholar
• Ito G, Okai T, Fujino G et al. GTP binding is essential to the protein kinase activity of LRRK2, a causative gene product for familial Parkinson’s disease. Biochemistry46(5), 1380–1388 (2007).
   PubMed Web of Science ®Google Scholar
• Di Fonzo A, Wu-Chou YH, Lu CS et al. A common missense variant in the LRRK2 gene, Gly2385Arg, associated with Parkinson’s disease risk in Taiwan. Neurogenetics7(3), 133–138 (2006).
   Google Scholar
• Tan EK, Peng R, Wu YR et al. LRRK2 G2385R modulates age at onset in Parkinson’s disease: a multi-center pooled analysis. Am. J. Med. Genet. B. Neuropsychiatr. Genet.150B(7), 1022–1023 (2009).
   Google Scholar
• Ross OA, Wu YR, Lee MC et al. Analysis of Lrrk2 R1628P as a risk factor for Parkinson’s disease. Ann. Neurol.64(1), 88–92 (2008).
   Google Scholar
• Scott WK, Nance MA, Watts RL et al. Complete genomic screen in Parkinson disease: evidence for multiple genes. JAMA286(18), 2239–2244 (2001).
   PubMed Web of Science ®Google Scholar
• Tobin JE, Latourelle JC, Lew MF et al. Haplotypes and gene expression implicate the MAPT region for Parkinson disease: the GenePD Study. Neurology71(1), 28–34 (2008).
   PubMedGoogle Scholar
• Zabetian CP, Hutter CM, Factor SA et al. Association analysis of MAPT H1 haplotype and subhaplotypes in Parkinson’s disease. Ann. Neurol.62(2), 137–144 (2007).
   Google Scholar
• Healy DG, Abou-Sleiman PM, Lees AJ et al. Tau gene and Parkinson’s disease: a case–control study and meta-analysis. J. Neurol. Neurosurg. Psychiatry75(7), 962–965 (2004).
   PubMed Web of Science ®Google Scholar
• Edwards TL, Scott WK, Almonte C et al. Genome-wide association study confirms SNPs in SNCA and the MAPT region as common risk factors for Parkinson disease. Ann. Hum. Genet.74(2), 97–109 (2010).
   PubMed Web of Science ®Google Scholar
• Mata IF, Samii A, Schneer SH et al. Glucocerebrosidase gene mutations: a risk factor for Lewy body disorders. Arch. Neurol.65(3), 379–382 (2008).
   PubMedGoogle Scholar
• Sidransky E, Nalls MA, Aasly JO et al. Multicenter analysis of glucocerebrosidase mutations in Parkinson’s disease. N. Engl. J. Med.361(17), 1651–1661 (2009).
   PubMed Web of Science ®Google Scholar
• Di Fonzo A, Dekker MC, Montagna P et al. FBXO7 mutations cause autosomal recessive, early-onset parkinsonian-pyramidal syndrome. Neurology72(3), 240–245 (2009).
   PubMed Web of Science ®Google Scholar
• Gregory A, Westaway SK, Holm IE et al. Neurodegeneration associated with genetic defects in phospholipase A(2). Neurology71(18), 1402–1409 (2008).
   PubMed Web of Science ®Google Scholar
• Tan EK, Khajavi M, Thornby JI, Nagamitsu S, Jankovic J, Ashizawa T. Variability and validity of polymorphism association studies in Parkinson’s disease. Neurology55(4), 533–538 (2000).
   PubMed Web of Science ®Google Scholar
• Satake W, Nakabayashi Y, Mizuta I et al. Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson’s disease. Nat. Genet.41(12), 1303–1307 (2009).
   PubMed Web of Science ®Google Scholar
• Simón-Sánchez J, Schulte C, Bras JM et al. Genome-wide association study reveals genetic risk underlying Parkinson’s disease. Nat. Genet.41(12), 1308–1312 (2009).
   PubMed Web of Science ®Google Scholar