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References

Published online by Cambridge University Press:  29 June 2020

Alberto Espay
Affiliation:
University of Cincinnati
Benjamin Stecher
Affiliation:
Educational Consultant and Healthcare Advocate
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Brain Fables
The Hidden History of Neurodegenerative Diseases and a Blueprint to Conquer Them
, pp. 151 - 159
Publisher: Cambridge University Press
Print publication year: 2020

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References

Calne, DB, Mizuno, Y. The neuromythology of Parkinson’s Disease. Parkinsonism Relat Disord. 2004;10(5):319322.Google Scholar
Postuma, RB, Berg, D, Stern, M, et al. MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord. 2015;30(12):15911601.Google Scholar
Espay, AJ, Schwarzschild, MA, Tanner, CM, et al. Biomarker-driven phenotyping in Parkinson’s disease: a translational missing link in disease-modifying clinical trials. Mov Disord. 2017;32(3):319324.CrossRefGoogle ScholarPubMed
Espay, AJ, Vizcarra, JA, Marsili, L, et al. Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases. Neurology. 2019;92(7):329337.CrossRefGoogle ScholarPubMed
Goetz, CG. Charcot on Parkinson’s disease. Mov Disord. 1986;1(1):2732.CrossRefGoogle ScholarPubMed
Lees, AJ. Unresolved issues relating to the shaking palsy on the celebration of James Parkinson’s 250th birthday. Mov Disord. 2007;22 Suppl 17:S327334.Google Scholar
Langston, JW, Palfreman, J. The Case of the Frozen Addicts. The Netherlands: IOS Press BV; 2014.Google Scholar
Langston, JW. The MPTP story. J Parkinsons Dis. 2017;7(s1):S11S19.Google Scholar
Langston, JW, Ballard, P, Tetrud, JW, Irwin, I. Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science. 1983;219(4587):979980.Google Scholar
McCormack, AL, Thiruchelvam, M, Manning-Bog, AB, et al. Environmental risk factors and Parkinson’s disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat. Neurobiol Dis. 2002;10(2):119127.CrossRefGoogle ScholarPubMed
Golbe, LI, Di Iorio, G, Bonavita, V, Miller, DC, Duvoisin, RC. A large kindred with autosomal dominant Parkinson’s disease. Ann Neurol. 1990;27(3):276282.Google Scholar
Polymeropoulos, MH, Higgins, JJ, Golbe, LI, et al. Mapping of a gene for Parkinson’s disease to chromosome 4q21-q23. Science. 1996;274(5290):11971199.Google Scholar
Polymeropoulos, MH, Lavedan, C, Leroy, E, et al. Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease. Science. 1997;276(5321):20452047.CrossRefGoogle ScholarPubMed
Spillantini, MG, Schmidt, ML, Lee, VM, et al. Alpha-synuclein in Lewy bodies. Nature. 1997;388(6645):839840.Google Scholar
Nussbaum, RL. The identification of alpha-synuclein as the first Parkinson disease gene. J Parkinsons Dis. 2017;7(s1):S43S49.CrossRefGoogle ScholarPubMed
Braak, H, Del Tredici, K, Rub, U, et al. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging. 2003;24(2):197211.Google Scholar
Shannon, KM, Keshavarzian, A, Mutlu, E, et al. Alpha-synuclein in colonic submucosa in early untreated Parkinson’s disease. Mov Disord. 2012;27(6):709715.Google Scholar
Shannon, KM, Keshavarzian, A, Dodiya, HB, Jakate, S, Kordower, JH. Is alpha-synuclein in the colon a biomarker for premotor Parkinson’s disease? Evidence from 3 cases. Mov Disord. 2012;27(6):716719.CrossRefGoogle Scholar
Berg, D, Postuma, RB, Adler, CH, et al. MDS research criteria for prodromal Parkinson’s disease. Mov Disord. 2015;30(12):16001611.Google Scholar
Luk, KC, Lee, VM. Modeling Lewy pathology propagation in Parkinson’s disease. Parkinsonism Relat Disord. 2014;20 Suppl 1:S85S87.Google Scholar
Olanow, CW, Prusiner, SB. Is Parkinson’s disease a prion disorder? Proc Natl Acad Sci U S A. 2009;106(31):1257112572.Google Scholar
Olanow, CW. Do prions cause Parkinson disease?: the evidence accumulates. Ann Neurol. 2014;75(3):331333.Google Scholar
Parkkinen, L, Kauppinen, T, Pirttila, T, Autere, JM, Alafuzoff, I. Alpha-synuclein pathology does not predict extrapyramidal symptoms or dementia. Ann Neurol. 2005;57(1):8291.CrossRefGoogle ScholarPubMed
Mikolaenko, I, Pletnikova, O, Kawas, CH, et al. Alpha-synuclein lesions in normal aging, Parkinson disease, and Alzheimer disease: evidence from the Baltimore Longitudinal Study of Aging (BLSA). J Neuropathol Exp Neurol. 2005;64(2):156162.CrossRefGoogle ScholarPubMed
Saito, Y, Ruberu, NN, Sawabe, M, et al. Lewy body-related alpha-synucleinopathy in aging. J Neuropathol Exp Neurol. 2004;63(7):742749.CrossRefGoogle ScholarPubMed
Ding, ZT, Wang, Y, Jiang, YP, et al. Characteristics of alpha-synucleinopathy in centenarians. Acta Neuropathol. 2006;111(5):450458.Google Scholar
Burke, RE, Dauer, WT, Vonsattel, JP. A critical evaluation of the Braak staging scheme for Parkinson’s disease. Ann Neurol. 2008;64(5):485491.Google Scholar
Jellinger, KA. A critical reappraisal of current staging of Lewy-related pathology in human brain. Acta Neuropathol. 2008;116(1):116.CrossRefGoogle ScholarPubMed
Zaccai, J, Brayne, C, McKeith, I, Matthews, F, Ince, PG. Patterns and stages of alpha-synucleinopathy: relevance in a population-based cohort. Neurology. 2008;70(13):10421048.CrossRefGoogle Scholar
Fujita, KA, Ostaszewski, M, Matsuoka, Y, et al. Integrating pathways of Parkinson’s disease in a molecular interaction map. Mol Neurobiol. 2014;49(1):88102.CrossRefGoogle Scholar
Nalls, MA, Blauwendraat, C, Vallerga, CL, et al. Identification of novel risk loci, causal insights, and heritable risk for Parkinson’s disease: a meta-analysis of genome-wide association studies. Lancet Neurol. 2019;18(12):10911102.CrossRefGoogle ScholarPubMed
Iwaki, H, Blauwendraat, C, Leonard, HL, et al. Genomewide association study of Parkinson’s disease clinical biomarkers in 12 longitudinal patients’ cohorts. Mov Disord. 2019;34(12):1839–1850.Google Scholar
Espay, AJ, Brundin, P, Lang, AE. Precision medicine for disease modification in Parkinson disease. Nat Rev Neurol. 2017;13(2):119126.Google Scholar
Crick, F. Central dogma of molecular biology. Nature. 1970;227(5258):561563.Google Scholar
Osler, W. The Principles and Practice of Medicine. NY: Appleton; 1892.Google Scholar
Grocott, MP. Integrative physiology and systems biology: reductionism, emergence and causality. Extrem Physiol Med. 2013;2(1):9.Google Scholar
Espay, AJ, Lang, AE. Parkinson diseases in the 2020s and beyond: replacing clinico-pathologic convergence with systems biology divergence. J Parkinsons Dis. 2018;8(s1):S59S64.CrossRefGoogle ScholarPubMed
Espay, AJ. The final nail in the coffin of disease modification for dopaminergic therapies: the LEAP Trial. JAMA Neurol. 2019;76(7):747748.CrossRefGoogle ScholarPubMed
Fahn, S, Oakes, D, Shoulson, I, et al. Levodopa and the progression of Parkinson’s disease. N Engl J Med. 2004;351(24):24982508.Google ScholarPubMed
Verschuur, CVM, Suwijn, SR, Boel, JA, et al. Randomized delayed-start trial of levodopa in Parkinson’s Disease. N Engl J Med. 2019;380(4):315324.Google Scholar
Zetusky, WJ, Jankovic, J, Pirozzolo, FJ. The heterogeneity of Parkinson’s disease: clinical and prognostic implications. Neurology. 1985;35(4):522526.Google Scholar
Simuni, T, Caspell-Garcia, C, Coffey, C, et al. How stable are Parkinson’s disease subtypes in de novo patients: analysis of the PPMI cohort? Parkinsonism Relat Disord. 2016;28:6267.CrossRefGoogle ScholarPubMed
Eisinger, RS, Hess, CW, Martinez-Ramirez, D, et al. Motor subtype changes in early Parkinson’s disease. Parkinsonism Relat Disord. 2017;43:6772.CrossRefGoogle ScholarPubMed
Marras, C, Lang, A. Parkinson’s disease subtypes: lost in translation? J Neurol Neurosurg Psychiatry. 2013;84(4):409415.Google Scholar
Mestre, TA, Eberly, S, Tanner, C, et al. Reproducibility of data-driven Parkinson’s disease subtypes for clinical research. Parkinsonism Relat Disord. 2018;56:102106.CrossRefGoogle ScholarPubMed
Fereshtehnejad, SM, Zeighami, Y, Dagher, A, Postuma, RB. Clinical criteria for subtyping Parkinson’s disease: biomarkers and longitudinal progression. Brain. 2017;140(7):19591976.CrossRefGoogle ScholarPubMed
De Pablo-Fernandez, E, Lees, AJ, Holton, JL, Warner, TT. Prognosis and neuropathologic correlation of clinical subtypes of Parkinson disease. JAMA Neurol. 2019;76(4):470479.Google Scholar
Espay, AJ, Marras, C. Clinical Parkinson disease subtyping does not predict pathology. Nat Rev Neurol. 2019;15(4):189190.Google Scholar
Sorensen, AA, Weedon, D. Productivity and impact of the top 100 cited Parkinson’s disease investigators since 1985. J Parkinsons Dis. 2011;1(1):313.Google Scholar
Buchman, AS, Yu, L, Wilson, RS, et al. Progressive parkinsonism in older adults is related to the burden of mixed brain pathologies. Neurology. 2019;92(16):e1821e1830.Google Scholar
Perl, DP, Olanow, CW, Calne, D. Alzheimer’s disease and Parkinson’s disease: distinct entities or extremes of a spectrum of neurodegeneration? Ann Neurol. 1998;44(3 Suppl 1):S19S31.Google Scholar
Irwin, DJ, Grossman, M, Weintraub, D, et al. Neuropathological and genetic correlates of survival and dementia onset in synucleinopathies: a retrospective analysis. Lancet Neurol. 2017;16(1):5565.CrossRefGoogle ScholarPubMed
McKeith, IG, Dickson, DW, Lowe, J, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology. 2005;65(12):18631872.Google Scholar
Devine, MJ, Gwinn, K, Singleton, A, Hardy, J. Parkinson’s disease and alpha-synuclein expression. Mov Disord. 2011;26(12):21602168.Google Scholar
Garcia-Ruiz, PJ, Espay, AJ. Parkinson disease: an evolutionary perspective. Front Neurol. 2017;8:157.Google Scholar
Ko, WKD, Bezard, E. Experimental animal models of Parkinson’s disease: a transition from assessing symptomatology to alpha-synuclein targeted disease modification. Exp Neurol. 2017;298(Pt B):172179.Google Scholar
Buttner, S, Broeskamp, F, Sommer, C, et al. Spermidine protects against alpha-synuclein neurotoxicity. Cell Cycle 2014;13(24):39033908.Google Scholar
Bergstrom, AL, Kallunki, P, Fog, K. Development of passive immunotherapies for synucleinopathies. Mov Disord. 2016;31(2):203213.Google Scholar
Fedak, KM, Bernal, A, Capshaw, ZA, Gross, S. Applying the Bradford Hill criteria in the 21st century: how data integration has changed causal inference in molecular epidemiology. Emerg Themes Epidemiol. 2015;12:14.Google Scholar
Hill, AB. The environment and disease: association or causation? 1965. J R Soc Med. 2015;108(1):3237.Google Scholar
Janec, E, Burke, RE. Naturally occurring cell death during postnatal development of the substantia nigra pars compacta of rat. Mol Cell Neurosci. 1993;4(1):3035.Google Scholar
Jeon, BS, Kholodilov, NG, Oo, TF, et al. Activation of caspase-3 in developmental models of programmed cell death in neurons of the substantia nigra. J Neurochem. 1999;73(1):322333.Google Scholar
Kholodilov, NG, Neystat, M, Oo, TF, et al. Increased expression of rat synuclein in the substantia nigra pars compacta identified by mRNA differential display in a model of developmental target injury. J Neurochem. 1999;73(6):25862599.CrossRefGoogle Scholar
Kholodilov, NG, Oo, TF, Burke, RE. Synuclein expression is decreased in rat substantia nigra following induction of apoptosis by intrastriatal 6-hydroxydopamine. Neurosci Lett. 1999;275(2):105108.Google Scholar
Stefanis, L, Kholodilov, N, Rideout, HJ, Burke, RE, Greene, LA. Synuclein-1 is selectively up-regulated in response to nerve growth factor treatment in PC12 cells. J Neurochem. 2001;76(4):11651176.Google Scholar
Burke, RE. alpha-Synuclein and parkin: coming together of pieces in puzzle of Parkinson’s disease. Lancet. 2001;358(9293):15671568.Google Scholar
Kitada, T, Asakawa, S, Hattori, N, et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature. 1998;392(6676):605608.Google Scholar
Stefanis, L, Wang, Q, Oo, T, et al. Lack of alpha-synuclein does not alter apoptosis of neonatal catecholaminergic neurons. Eur J Neurosci. 2004;20(7):19691972.Google Scholar
Cohen, AD, Landau, SM, Snitz, BE, et al. Fluid and PET biomarkers for amyloid pathology in Alzheimer’s disease. Mol Cell Neurosci. 2018;97:3-17.Google Scholar
Wang, J, Dickson, DW, Trojanowski, JQ, Lee, VM. The levels of soluble versus insoluble brain Abeta distinguish Alzheimer’s disease from normal and pathologic aging. Exp Neurol. 1999;158(2):328337.Google Scholar
Gilman, S, Koller, M, Black, RS, et al. Clinical effects of Abeta immunization (AN1792) in patients with AD in an interrupted trial. Neurology. 2005;64(9):15531562.Google Scholar
Ostrowitzki, S, Lasser, RA, Dorflinger, E, et al. A phase III randomized trial of gantenerumab in prodromal Alzheimer’s disease. Alzheimers Res Ther. 2017;9(1):95.Google Scholar
Salloway, S, Sperling, R, Fox, NC, et al. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer’s disease. N Engl J Med. 2014;370(4):322333.Google Scholar
Doody, RS, Raman, R, Farlow, M, et al. A phase 3 trial of semagacestat for treatment of Alzheimer’s disease. N Engl J Med. 2013;369(4):341350.Google Scholar
Doody, RS, Thomas, RG, Farlow, M, et al. Phase 3 trials of solanezumab for mild-to-moderate Alzheimer’s disease. N Engl J Med. 2014;370(4):311321.Google Scholar
Honig, LS, Vellas, B, Woodward, M, et al. Trial of solanezumab for mild dementia due to Alzheimer’s disease. N Engl J Med. 2018;378(4):321330.Google Scholar
Ingelsson, M. alpha-Synuclein oligomers-neurotoxic molecules in Parkinson’s disease and other Lewy body disorders. Front Neurosci. 2016;10:408.CrossRefGoogle ScholarPubMed
Polvikoski, T, Sulkava, R, Myllykangas, L, et al. Prevalence of Alzheimer’s disease in very elderly people: a prospective neuropathological study. Neurology. 2001;56(12):16901696.CrossRefGoogle ScholarPubMed
Markesbery, WR, Jicha, GA, Liu, H, Schmitt, FA. Lewy body pathology in normal elderly subjects. J Neuropathol Exp Neurol. 2009;68(7):816822.Google Scholar
Balasubramanian, AB, Kawas, CH, Peltz, CB, Brookmeyer, R, Corrada, MM. Alzheimer disease pathology and longitudinal cognitive performance in the oldest-old with no dementia. Neurology. 2012;79(9):915921.Google Scholar
Silver, MH, Newell, K, Brady, C, Hedley-White, ET, Perls, TT. Distinguishing between neurodegenerative disease and disease-free aging: correlating neuropsychological evaluations and neuropathological studies in centenarians. Psychosom Med. 2002;64(3):493501.CrossRefGoogle ScholarPubMed
Berlau, DJ, Corrada, MM, Head, E, Kawas, CH. APOE epsilon2 is associated with intact cognition but increased Alzheimer pathology in the oldest old. Neurology. 2009;72(9):829834.Google Scholar
Kawas, CH, Kim, RC, Sonnen, JA, et al. Multiple pathologies are common and related to dementia in the oldest-old: the 90+ Study. Neurology. 2015;85(6):535542.Google Scholar
Latimer, CS, Keene, CD, Flanagan, ME, et al. Resistance to Alzheimer disease neuropathologic changes and apparent cognitive resilience in the Nun and Honolulu-Asia Aging Studies. J Neuropathol Exp Neurol. 2017;76(6):458466.Google Scholar
Robinson, JL, Corrada, MM, Kovacs, GG, et al. Non-Alzheimer’s contributions to dementia and cognitive resilience in the 90+ Study. Acta Neuropathol. 2018;136(3):377388.Google Scholar
Ueda, K, Fukushima, H, Masliah, E, et al. Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease. Proc Natl Acad Sci U S A. 1993;90(23):1128211286.Google Scholar
Iwai, A, Yoshimoto, M, Masliah, E, Saitoh, T. Non-A beta component of Alzheimer’s disease amyloid (NAC) is amyloidogenic. Biochemistry. 1995;34(32):1013910145.Google Scholar
Sardi, SP, Clarke, J, Kinnecom, C, et al. CNS expression of glucocerebrosidase corrects alpha-synuclein pathology and memory in a mouse model of Gaucher-related synucleinopathy. Proc Natl Acad Sci U S A. 2011;108(29):1210112106.Google Scholar
Parkkinen, L, O’Sullivan, SS, Collins, C, et al. Disentangling the relationship between lewy bodies and nigral neuronal loss in Parkinson’s disease. J Parkinsons Dis. 2011;1(3):277286.Google Scholar
Hay, J, Johnson, VE, Smith, DH, Stewart, W. Chronic traumatic encephalopathy: the neuropathological legacy of traumatic brain injury. Annu Rev Pathol. 2016;11:2145.Google Scholar
Farah, G, Siwek, D, Cummings, P. Tau accumulations in the brains of woodpeckers. PLoS One. 2018;13(2):e0191526.Google Scholar
The Hope List: Parkinson’s Therapies in Development. 2019. https://drive.google.com/file/d/1NeSyFA37b9IbUzryRRP-EqrgScjCRL-3/view. Accessed January 2020.Google Scholar
Dumurgier, J, Hanseeuw, BJ, Hatling, FB, et al. Alzheimer’s disease biomarkers and future decline in cognitive normal older adults. J Alzheimers Dis. 2017;60(4):14511459.CrossRefGoogle ScholarPubMed
Payami, H. The emerging science of precision medicine and pharmacogenomics for Parkinson’s disease. Mov Disord. 2017;32(8):11391146.Google Scholar
Mollenhauer, B, Caspell-Garcia, CJ, Coffey, CS, et al. Longitudinal CSF biomarkers in patients with early Parkinson disease and healthy controls. Neurology. 2017;89(19):1959-1969.Google Scholar
Skillback, T, Mattsson, N, Hansson, K, et al. A novel quantification-driven proteomic strategy identifies an endogenous peptide of pleiotrophin as a new biomarker of Alzheimer’s disease. Sci Rep. 2017;7(1):13333.Google Scholar
Dumurgier, J, Hanseeuw, BJ, Hatling, FB, et al. Alzheimer’s disease biomarkers and future decline in cognitive normal older adults. J Alzheimers Dis. 2017;60(4):14511459.Google Scholar
Postuma, RB, Poewe, W, Litvan, I, et al. Validation of the MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord. 2018;33(10):16011608.Google Scholar
Berg, D, Adler, CH, Bloem, BR, et al. Movement disorder society criteria for clinically established early Parkinson’s disease. Mov Disord. 2018;33(10):16431646.Google Scholar
Kang, JH, Mollenhauer, B, Coffey, CS, et al. CSF biomarkers associated with disease heterogeneity in early Parkinson’s disease: the Parkinson’s Progression Markers Initiative study. Acta Neuropathol. 2016;131(6):935949.CrossRefGoogle ScholarPubMed
Mollenhauer, B, Zimmermann, J, Sixel-Doring, F, et al. Monitoring of 30 marker candidates in early Parkinson disease as progression markers. Neurology. 2016;87(2):168177.Google Scholar
Thenganatt, MA, Jankovic, J. Parkinson disease subtypes. JAMA Neurol. 2014;71(4):499504.Google Scholar
Zhu, K, van Hilten, JJ, Marinus, J. Predictors of dementia in Parkinson’s disease; findings from a 5-year prospective study using the SCOPA-COG. Parkinsonism Relat Disord. 2014;20(9):980985.CrossRefGoogle ScholarPubMed
Terrelonge, M, Jr., Marder, KS, Weintraub, D, Alcalay, RN. CSF beta-amyloid 1–42 predicts progression to cognitive impairment in newly diagnosed Parkinson disease. J Mol Neurosci. 2016;58(1):8892.CrossRefGoogle ScholarPubMed
Parnetti, L, Gaetani, L, Eusebi, P, et al. CSF and blood biomarkers for Parkinson’s disease. Lancet Neurol. 2019;18(6):573586.CrossRefGoogle ScholarPubMed
Zhang, J, Mattison, HA, Liu, C, et al. Longitudinal assessment of tau and amyloid beta in cerebrospinal fluid of Parkinson disease. Acta Neuropathol. 2013;126(5):671682.Google Scholar
Parnetti, L, Chiasserini, D, Persichetti, E, et al. Cerebrospinal fluid lysosomal enzymes and alpha-synuclein in Parkinson’s disease. Mov Disord. 2014;29(8):10191027.Google Scholar
Parnetti, L, Paciotti, S, Eusebi, P, et al. Cerebrospinal fluid beta-glucocerebrosidase activity is reduced in Parkinson’s disease patients. Mov Disord. 2017;32(10):14231431.Google Scholar
Majbour, NK, Vaikath, NN, Eusebi, P, et al. Longitudinal changes in CSF alpha-synuclein species reflect Parkinson’s disease progression. Mov Disord. 2016;31(10):15351542.Google Scholar
Constantinides, VC, Paraskevas, GP, Emmanouilidou, E, et al. CSF biomarkers beta-amyloid, tau proteins and a-synuclein in the differential diagnosis of Parkinson-plus syndromes. J Neurol Sci. 2017;382:9195.Google Scholar
Backstrom, DC, Eriksson Domellof, M, Linder, J, et al. Cerebrospinal fluid patterns and the risk of future dementia in early, incident Parkinson disease. JAMA Neurol. 2015;72(10):11751182.Google Scholar
Chiasserini, D, Biscetti, L, Eusebi, P, et al. Differential role of CSF fatty acid binding protein 3, alpha-synuclein, and Alzheimer’s disease core biomarkers in Lewy body disorders and Alzheimer’s dementia. Alzheimers Res Ther. 2017;9(1):52.Google Scholar
Chen-Plotkin, AS, Albin, R, Alcalay, R, et al. Finding useful biomarkers for Parkinson’s disease. Sci Transl Med. 2018;10(454):pii: eaam6003.Google Scholar
Palfreman, J. Brain Storms. Canada: Harper Collins; 2015.Google Scholar
Veronesi, U, Saccozzi, R, Del Vecchio, M, et al. Comparing radical mastectomy with quadrantectomy, axillary dissection, and radiotherapy in patients with small cancers of the breast. N Engl J Med. 1981;305(1):611.Google Scholar
Pharmaceutical Research and Manufacturers of America 2018; http://phrma-docs.phrma.org/files/dmfile/AlzheimersSetbacksSteppingStones_FINAL_digital.pdf. Accessed January 2020.Google Scholar
Halsted, WS. I. A clinical and histological study of certain adenocarcinomata of the breast: and a brief consideration of the supraclavicular operation and of the results of operations for cancer of the breast from 1889 to 1898 at the Johns Hopkins Hospital. Ann Surg. 1898;28(5):557576.Google Scholar
Veronesi, U, Cascinelli, N, Mariani, L, et al. Twenty-year follow-up of a randomized study comparing breast-conserving surgery with radical mastectomy for early breast cancer. N Engl J Med. 2002;347(16):12271232.Google Scholar
Malhotra, GK, Zhao, X, Band, H, Band, V. Histological, molecular and functional subtypes of breast cancers. Cancer Biol Ther. 2010;10(10):955960.Google Scholar
Bianchini, G, Balko, JM, Mayer, IA, Sanders, ME, Gianni, L. Triple-negative breast cancer: challenges and opportunities of a heterogeneous disease. Nat Rev Clin Oncol. 2016;13(11):674690.Google Scholar
The Economist. European countries demand that publicly funded research be free. www.economist.com/science-and-technology/2018/09/15/european-countries-demand-that-publicly-funded-research-be-free. Accessed January 2020.Google Scholar
Gold, ER. Should Universities Get Out Of The Patent Business? 2019; www.cigionline.org/articles/should-universities-get-out-patent-business. Accessed January 2020.Google Scholar
Perry, TL, Godin, DV, Hansen, S. Parkinson’s disease: a disorder due to nigral glutathione deficiency? Neurosci Lett. 1982;33(3):305310.Google Scholar
Shults, CW, Haas, RH, Beal, MF. A possible role of coenzyme Q10 in the etiology and treatment of Parkinson’s disease. Biofactors. 1999;9(2–4):267272.CrossRefGoogle ScholarPubMed
Parain, K, Murer, MG, Yan, Q, et al. Reduced expression of brain-derived neurotrophic factor protein in Parkinson’s disease substantia nigra. Neuroreport. 1999;10(3):557561.Google Scholar
Hunot, S, Bernard, V, Faucheux, B, et al. Glial cell line-derived neurotrophic factor (GDNF) gene expression in the human brain: a post mortem in situ hybridization study with special reference to Parkinson’s disease. J Neural Transm (Vienna). 1996;103(8–9):10431052.Google Scholar
Beal, MF, Oakes, D, Shoulson, I, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. 2014;71(5):543552.Google ScholarPubMed
Kieburtz, K, Tilley, BC, Elm, JJ, et al. Effect of creatine monohydrate on clinical progression in patients with Parkinson disease: a randomized clinical trial. JAMA. 2015;313(6):584593.Google Scholar
The Parkinson Study Group. Effect of deprenyl on the progression of disability in early Parkinson’s disease: the Parkinson Study Group. New Engl J Med. 1989;321(20):13641371.Google Scholar
Snow, BJ, Rolfe, FL, Lockhart, MM, et al. A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson’s disease. Mov Disord. 2010;25(11):16701674.Google Scholar
Writing Group for the NETiPDI, Kieburtz, K, Tilley, BC, et al. Effect of creatine monohydrate on clinical progression in patients with Parkinson disease: a randomized clinical trial. JAMA. 2015;313(6):584593.Google Scholar
Investigators N-PF-Z. Pioglitazone in early Parkinson’s disease: a phase 2, multicentre, double-blind, randomised trial. Lancet Neurol. 2015;14(8):795803.Google Scholar
Rascol, O, Olanow, CW, Brooks, D, et al. A 2-year multicenter, placebo-controlled, double-blind, parallel group study of the effect of riluzole on Parkinson’s disease progression. Mov Disord. 2002;17(Suppl 5):39.Google Scholar
Shults, CW. Effect of selegiline (deprenyl) on the progression of disability in early Parkinson’s disease: Parkinson Study Group. Acta Neurol Scand Suppl. 1993;146:3642.Google Scholar
Parkinson Study Group QE3 Investigtors, Beal, MF, Oakes, D, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. 2014;71(5):543552.Google Scholar
Myllyla, VV, Sotaniemi, KA, Vuorinen, JA, Heinonen, EH. Selegiline as initial treatment in de novo parkinsonian patients. Neurology. 1992;42(2):339343.Google Scholar
Olanow, CW, Rascol, O, Hauser, R, et al. A double-blind, delayed-start trial of rasagiline in Parkinson’s disease. N Engl J Med. 2009;361(13):12681278.Google Scholar
Schapira, AH, McDermott, MP, Barone, P, et al. Pramipexole in patients with early Parkinson’s disease (PROUD): a randomised delayed-start trial. Lancet Neurol. 2013;12(8):747755.Google Scholar
Hauser, RA, Lyons, KE, McClain, T, Carter, S, Perlmutter, D. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson’s disease. Mov Disord. 2009;24(7):979983.Google Scholar
Olanow, W, Bartus, RT, Baumann, TL, et al. Gene delivery of neurturin to putamen and substantia nigra in Parkinson disease: a double-blind, randomized, controlled trial. Ann Neurol. 2015;78(2):248257.CrossRefGoogle Scholar
Lang, AE, Gill, S, Patel, NK, et al. Randomized controlled trial of intraputamenal glial cell line-derived neurotrophic factor infusion in Parkinson disease. Ann Neurol. 2006;59(3):459466.Google Scholar
Ribeiro, MJ, Stoessl, AJ, Brooks, D. Evaluation of a potential neurotrophic drug on the progression of Parkinson disease with 18FDOPA. J Nucl Med. 2006;50(Suppl. 2):A125.Google Scholar
NINDS NET-PD Investigators. A randomized, double-blind, futility clinical trial of creatine and minocycline in early Parkinson disease. Neurology. 2006;66(5):664671.Google Scholar
GPI 1485 Study Group. GPI 1485, a neuroimmunophilin ligand, fails to alter disease progression in mild to moderate Parkinson’s disease. Mov Disord. 2006;21:A1009.Google Scholar
Olanow, CW, Schapira, AH, LeWitt, PA, et al. TCH346 as a neuroprotective drug in Parkinson’s disease: a double-blind, randomised, controlled trial. Lancet Neurol. 2006;5(12):10131020.Google Scholar
Parkinson Study Group. Mixed lineage kinase inhibitor CEP-1347 fails to delay disability in early Parkinson disease. Neurology. 2007;69(15):14801490.Google Scholar
Kaiser, J. The Alzheimer’s gamble. Science. 2018;361(6405):838841.Google Scholar
Panza, F, Lozupone, M, Logroscino, G, Imbimbo, BP. A critical appraisal of amyloid-beta-targeting therapies for Alzheimer disease. Nat Rev Neurol. 2019;15(2):7388.Google Scholar
Knopman, DS. Bad news and good news in AD, and how to reconcile them. Nat Rev Neurol. 2019;15(2):6162.Google Scholar
Cummings, JL, Cohen, S, van Dyck, CH, et al. ABBY: A phase 2 randomized trial of crenezumab in mild to moderate Alzheimer disease. Neurology. 2018;90(21):e1889e1897.CrossRefGoogle Scholar
Egan, MF, Kost, J, Tariot, PN, et al. Randomized trial of verubecestat for mild-to-moderate Alzheimer’s disease. N Engl J Med. 2018;378(18):16911703.Google Scholar
Biogen. Biogen Plans Regulatory Filing for Aducanumab in Alzheimer’s disease Based on New Analysis of Larger Dataset from Phase 3 Studies. http://investors.biogen.com/news-releases/news-release-details/biogen-plans-regulatory-filing-aducanumab-alzheimers-disease. Accessed January 2020.Google Scholar
Scheuerle, A. Limits of the genetic revolution. Arch Pediatr Adolesc Med. 2001;155(11):12041209.Google Scholar
Frisoni, GB, Ritchie, C, Carrera, E, et al. Re-aligning scientific and lay narratives of Alzheimer’s disease. Lancet Neurol. 2019;18(10):918919.Google Scholar
Kannel, WB. Framingham study insights into hypertensive risk of cardiovascular disease. Hypertens Res. 1995;18(3):181196.Google Scholar
Jack, CR, Jr., Bennett, DA, Blennow, K, et al. NIA-AA research framework: toward a biological definition of Alzheimer’s disease. Alzheimers Dement. 2018;14(4):535562.Google Scholar
Jack, CR, Jr., Therneau, TM, Weigand, SD, et al. Prevalence of biologically vs clinically defined Alzheimer spectrum entities using the National Institute on Aging-Alzheimer’s Association research framework. JAMA Neurol. 2019; Jul 15 (Epub ahead of print) (DOI:10.1001/jamaneurol.2019.1971).Google Scholar
Shokri-Kojori, E, Wang, GJ, Wiers, CE, et al. beta-Amyloid accumulation in the human brain after one night of sleep deprivation. Proc Natl Acad Sci U S A. 2018;115(17):44834488.Google Scholar
Xie, L, Kang, H, Xu, Q, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342(6156):373377.Google Scholar
Riordan, JR, Rommens, JM, Kerem, B, et al. Identification of the cystic fibrosis gene: cloning and characterization of complementary DNA. Science. 1989;245(4922):10661073.Google Scholar
Flume, PA, Liou, TG, Borowitz, DS, et al. Ivacaftor in subjects with cystic fibrosis who are homozygous for the F508del-CFTR mutation. Chest. 2012;142(3):718724.Google Scholar
Accurso, FJ, Rowe, SM, Clancy, JP, et al. Effect of VX-770 in persons with cystic fibrosis and the G551D-CFTR mutation. N Engl J Med. 2010;363(21):19912003.Google Scholar
Ramsey, BW, Davies, J, McElvaney, NG, et al. A CFTR potentiator in patients with cystic fibrosis and the G551D mutation. N Engl J Med. 2011;365(18):16631672.Google Scholar
Dorsey, ER, Sherer, T, Okun, MS, Bloem, BR. The emerging evidence of the Parkinson pandemic. J Parkinsons Dis. 2018;8(s1):S3-S8.Google Scholar
Brockman, JE. This Idea Must Die: Scientific Theories That Are Blocking Progress. New York: HarperCollins Publishers; 2015.Google Scholar
Cedarbaum, JM. Elephants, Parkinson’s disease, and proof-of-concept clinical trials. Mov Disord. 2018;33(5):697700.Google Scholar
Lang, AE, Espay, AJ. Disease modification in Parkinson’s disease: current approaches, challenges, and future considerations. Mov Disord. 2018;33(5):660677.Google Scholar
The Australian Parkinson’s Mission. 2019; https://scienceofparkinsons.com/2019/01/30/apm/. Accessed January 2020.Google Scholar
Chan Zuckerbert Initiative. 2019; https://chanzuckerberg.com/science/. Accessed January 2020.Google Scholar
Chan Zuckerberg Initiative. Human Cell Atlas. https://chanzuckerberg.com/science/programs-resources/humancellatlas/. Accessed January 2020.Google Scholar
Raudino, F. The Parkinson disease before James Parkinson. Neurol Sci. 2012;33(4):945948.Google Scholar

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