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Amyotrophic Lateral Sclerosis, Parkinson’s Disease and Alzheimer’s Disease: Phylogenetic Disorders of the Human Neocortex Sharing Many Characteristics

Published online by Cambridge University Press:  18 September 2015

Andrew Eisen  and
Donald Calne
Andrew Eisen*
Affiliation:
“Neurodegenerative Disorders Centre” and the University of British Columbia, Vancouver
Donald Calne
Affiliation:
“Neurodegenerative Disorders Centre” and the University of British Columbia, Vancouver
*
The Neuromuscular Diseases Unit, Vancouver General Hospital, 855 West 12th Avenue, Vancouver, British Columbia, Canada V5Z 1M9
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Abstract:

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Features common to amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD) and Alzheimer’s disease (AD) are reviewed. Shared epidemiological aspects include an increasing frequency which is proportional for each disease. We draw attention to geographic non-uniform distribution which, for ALS and PD, correlates positively with latitude. Clinical and pathological overlap occurs in the same patients, and in members of the same family. A high early morning plasma cysteine/sulphate ratio possibly related to the development of proteinacious inclusions, as well as ubiquinated neuronal inclusions, characterize ALS, PD and AD. HLA-DR (the human group II major histocompatibility class) staining is marked in ALS, PD and AD and may represent autoimmunity-incited by-products of neuronal degeneration. Based upon demonstrated glutaminergic connections between the neocortex and anterior horn cells, the entorhinal cortex and the basal ganglia we hypothesize that ALS, AD and PD are phylogenetic disturbances of the neocortical cell. The postsynaptic neuron may degenerate secondarily to anterograde effects of deranged glutamate metabolism. Future therapeutic strategies should be directed to agents that decrease transmission induced by excitatory amino-acids.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 19 , Issue S1: 3rd Canadian Conference on Neurodegenerative Diseases , February 1992 , pp. 117 - 123
Copyright
Copyright © Canadian Neurological Sciences Federation 1992

References

1.Hudson, AJ, Amyotrophic lateral sclerosis and its association with dementia, parkinsonism and other neurological disorders: a review. Brain 1981; 104: 217–247.CrossRefGoogle ScholarPubMed
2.Hudson, AJ, Rice, GPA.Similarities of Guamanian ALS/PD to post-encephalitic parkinsonism/ALS: possible viral cause. Can J Neurol Sci 1990; 17: 427–433.CrossRefGoogle ScholarPubMed
3.Garruto, RM, Yanagihara, R, Gajdusek, DC.Disappearance of high-incidence amyotrophic lateral sclerosis and parkinsonian-dementia on Guam. Neurology 1985; 35: 193–198.CrossRefGoogle Scholar
4.Calne, DB, Lees, AJ.Late progression of post-encephalitic Parkinson’s syndrome. Can J Neurol Sci 1988; 15: 135–138.CrossRefGoogle ScholarPubMed
5.Brait, K, Fahn, S, Schwarz, GA.Sporadic and familial parkinsonism and motor neuron disease. Neurology 1973; 23: 990–1002.CrossRefGoogle ScholarPubMed
6.Calne, DB, Eisen, A, McGeer, E, et al. Alzheimer’s disease. Parkinson’s disease and motorneurone disease: a biotrophic interaction between aging and environment? Lancet 1986; II: 1067–1070.CrossRefGoogle Scholar
7.Calne, DB, Eisen, A.The relationship between Alzheimer’s disease, Parkinson’s disease and motor neuron disease. Can J Neurol Sci 1989; 16: 547–550.CrossRefGoogle ScholarPubMed
8.Calne, DB, Eisen, A.Parkinson’s disease, motoneuron disease and Alzheimer’s disease: origins and interrelationship. Adv Neurol 1990; 53: 355–360.Google ScholarPubMed
9.Rosser, MN.Parkinson’s disease and Alzheimer’s disease as disorders of the isodendritic core. Br Med J 1981; 283: 1588–1590.CrossRefGoogle Scholar
10.Appel, SH.A unifying hypothesis for the cause of amyotrophic lateral sclerosis, parkinsonism and Alzheimer’s disease. Ann Neurol 1981; 10: 499–505.CrossRefGoogle Scholar
11.Rocca, WA, Amaducci, LA, Schoenberg, BS.Epidemiology of clinically diagnosed Alzheimer’s disease. Ann Neurol 1986: 19: 415–424.CrossRefGoogle ScholarPubMed
12.Teravainen, H, Forgach, L, Hietanen, M, et al. The age of onset of Parkinson’s disease: etiological implications. Can J Neurol Sci 1986; 13: 317–319.CrossRefGoogle ScholarPubMed
13.Bayles, KA.Age of onset of Alzheimer’s disease. Arch Neurol 1991; 48: 155–159.CrossRefGoogle ScholarPubMed
14.Hudson, AJ.Amyotrophic lateral sclerosis: clinical evidence for differences in pathogenesis and etiology. In: Hudson, AJ, ed., Amyotrophic Lateral Sclerosis: Concepts in Pathogenesis and Etiology. Toronto: University of Toronto Press, 1990: 108–143.Google Scholar
15.Cuesta, JP.Studies on the prevalence of paralysis agitans by tracer methodology. PhD thesis; Departments of Social Medicine and Endocrinology, Karolinska Institute, Stockholm, Sweden. Huddinge 1986: 113.Google Scholar
16.Rajput, AH, Calne, D, Lang, AE.National Conference on Parkinson’s Disease – Conference summary. Can J Neurol Sci 1991; 18: 87–92.CrossRefGoogle Scholar
17.Bozek, C, Eisen, A.Acquired motor neuron disease of the young. Neurology 1985; 25 (Suppl I): 249.Google Scholar
18.Mukai, E, Sakakibara, T, Sobue, I.The relationship between prognosis and sex and age at onset in amyotrophic lateral sclerosis. Clin Neurol 1984; 24: 679–685.Google ScholarPubMed
19.Golbe, LI.Young-onset Parkinson’s disease: a clinical review. Neurology 1991; 41: 168–173.CrossRefGoogle ScholarPubMed
20.Lilenfeld, DE, Chan, E, Ehland, J, et al. Rising mortality for mononeuron disease in the USA, 1962–84. Lancet 1989; 1: 810–813.Google Scholar
21.Stallones, I, Kasarkis, EJ, Stipanowich, C, et al. Secular trends in mortality rates from motor neuron disease in Kentucky, 1964–1984. Neuroepidemiology 1989; 8: 68–78.CrossRefGoogle ScholarPubMed
22.Flaten, TP.Rising mortality from mononeuron disease. Lancet 1989; I: 1018–1019.CrossRefGoogle Scholar
23.Lilienfeld, DE, Chan, E, Ehland, J, et al. Two decades of increasing mortality from Parkinson’s diseases among US elderly. Arch Neurol 1990; 47: 731–734.CrossRefGoogle ScholarPubMed
24.Annegers, JF, Appel, S, Lee, JR, et al. Incidence and prevalence of amyotrophic lateral sclerosis in Harris County, Texas, 1985–1988. Arch Neurol 1991; 48: 589–593.CrossRefGoogle ScholarPubMed
25.Rocca, WA, Bonaiuto, S, Lippi, A, et al. Prevalence of clinically diagnosed Alzheimer’s disease and other dementing disorders: a door-to-door survey in Appignano, Macerata province, Italy. Neurology 1990; 40: 626–631.CrossRefGoogle ScholarPubMed
26.Calne, DB, Calne, JS.Normality and disease. Can J Neurol Sci 1988; 15: 3–4.CrossRefGoogle ScholarPubMed
27.Morris, JC, Drazner, M, Fulling, K, et al. Clinical and pathological aspects of parkinsonism and Alzheimer’s disease. Arch Neurol 1989; 46: 651–657.CrossRefGoogle Scholar
28.Strong, MJ, Hudson, AJ, Alvord, WG.Familial amyotrophic lateral sclerosis, 1850–1989: a statistical analysis of the world literature. Can J Neurol Sci 1991; 18: 46–58.CrossRefGoogle Scholar
29.Fitch, N, Backer, R, Heller, A.The inheritance of Alzheimer’s disease: a new interpretation. Ann Neurol 1988; 23: 14–19.CrossRefGoogle ScholarPubMed
30.Golbe, LI.The genetics of Parkinson’s disease: a reconsideration. Neurology 1990; 40 (Suppl 3): 7–14.Google ScholarPubMed
31.St George-Hyslop, P, Tanzi, R, Polinsky, R, et al. The genetic defect causing familial Alzheimer’s disease maps on chromosome 21. Science 1987; 235: 885–890.CrossRefGoogle ScholarPubMed
32.Siddique, T, Figlewicz, DA, Pericak-Vance, MA.Linkage of a gene causing familial amyotrophic lateral sclerosis to chromosome 21 and evidence for genetic locus heterogeneity. N Engl J Med (in press).Google Scholar
33.Golbe, LI, Dilorio, G, Bonavita, V, et al. A large kindred with autosomal dominant Parkinson’s diseases. Ann Neurol 1990; 27: 276–282.CrossRefGoogle Scholar
34.Poirier, J, Kogan, S, Gauthier, S.Environment, genetics and idiopathic Parkinson’s disease. Can J Neurol Sci 1991; 18: 70–76.CrossRefGoogle ScholarPubMed
35.Marsden, CD.Parkinson’s in twins. J Neurol Neurosurg Psychiatry 1987; 50: 105–106.CrossRefGoogle ScholarPubMed
36.Manila, RJ, Kaprio, J, Koskenvuo, M, et al. Parkinson’s in a nation-wide twin cohort. Neurology 1988; 38: 1217–1219.Google Scholar
37.Creasey, H, Jorm, A, Longley, W, et al. Monozygotic twins discordant for Alzheimer’s disease. Neurology 1989; 39: 1474–1476.CrossRefGoogle ScholarPubMed
38.Renvoize, EB, Mindham, RHS, Stewart, M, et al. Identical twins discordant for presenile dementia of the Alzheimer type. Br J Psychiatry 1986; 149: 509–512.CrossRefGoogle ScholarPubMed
39.Galasko, D, Kwo-on-Yuen, PF, Klauber, MR, et al. Neurological findings in Alzheimer’s disease and normal aging. Arch Neurol 1990; 47: 625–627.CrossRefGoogle ScholarPubMed
40.Leverenz, J, Sumi, SM.Parkinson’s disease in patients with Alzheimer’s disease. Arch Neurol 1986; 43: 662–664.CrossRefGoogle ScholarPubMed
41.Ditter, SM, Mirra, SS.Neuropathological and clinical features of Parkinson’s disease in Alzheimer’s disease patients. Neurology 1987; 37: 754–760.CrossRefGoogle ScholarPubMed
42.Boiler, F, Mizutani, T, Roessmann, U, et al. Parkinson’s disease, dementia and Alzheimer’s disease: clinicopathological correlations. Ann Neurol 1980; 7: 329–335.CrossRefGoogle Scholar
43.McGeer, PL, Itagski, S, Akiyama, H, et al. Rate of cell death in parkinsonism indicates active neuropathological process. Ann Neurol 1988; 24: 574–576.CrossRefGoogle ScholarPubMed
44.Joachim, CL, Morris, JH, Selkoe, DJ.Clinically diagnosed Alzheimer’s disease: autopsy results in 150 cases. Ann Neurol 1988; 24: 50–56.CrossRefGoogle ScholarPubMed
45.Gaspar, P, Gray, F.Dementia in idiopathic Parkinson’s disease: a neuropathological study of 32 cases. Acta Neuopathol 1984; 64: 43–52.CrossRefGoogle ScholarPubMed
46.Whitehouse, PJ.The concept of subcortical and cortical dementia: another look. Ann Neurol 1986; 19: 1–6.CrossRefGoogle ScholarPubMed
47.Gibb, WRG, Scott, T, Lees, AJ.Neuronal inclusions of Parkinson’s disease. Movement Disorders 1991; 6: 2–11.CrossRefGoogle ScholarPubMed
48.Price, DL, Whitehouse, PJ, Struble, RG.Cellular pathology in Alzheimer’s and Parkinson’s disease. Trends Neurosci 1986; 9: 29–33.CrossRefGoogle Scholar
49.Gibb, WR, Mountjoy, CQ, Mann, DM, et al. A pathological study of the association between Lewy body disease and Alzheimer’s disease. J Neurol Neurosurg Psychiatry 1989; 52: 701–708.CrossRefGoogle ScholarPubMed
50.Lennox, G, Lowe, JS, Godwin-Austin, RB, et al. Diffuse Lewy body disease: an important differential diagnosis in dementia with extrapyramidal features. Prog Clin Biol Res 1989; 317: 121–130.Google ScholarPubMed
51.Hansen, L, Salmon, D, Galasko, D, et al. The Lewy body variant of Alzheimer’s disease: a clinical and pathological entity. Neurology 1990; 40: 1–8.CrossRefGoogle Scholar
52.Crystal, HA, Dickson, DW, Lizardi, JE, et al. Antemortem diagnosis of diffuse Lewy body disease. Neurology 1990; 40: 1523–1528.CrossRefGoogle ScholarPubMed
53.Rajput, AH, Uitti, RJ, Sudhakar, S, et al. Parkinsonism and neurofibrillary tangle pathology in pigmented nuclei. Ann Neurol 1989; 25: 602–606.CrossRefGoogle ScholarPubMed
54.Deapen, DM, Henderson, BE.A case-control study of amyotrophic lateral sclerosis. Am J Epidemiol 1986; 123: 790–799.CrossRefGoogle ScholarPubMed
55.Mulder, DW, Kurland, LT, Offord, KP, et al. Familial adult motor neuron disease: amyotrophic lateral sclerosis. Neurology 1986; 36: 511–517.Google ScholarPubMed
56.Hofman, A, Schulte, W, Tanja, TA, et al. History of dementia and Parkinson’s disease in 1st-degree relatives of patients with Alzheimer’s disease. Neurology 1989; 39: 1589–1592.CrossRefGoogle ScholarPubMed
57.Heafield, MT, Fearn, S, Steventon, GB, et al. Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson’s and Alzheimer’s disease. Neurosci Lett 1990; 110: 216–220.CrossRefGoogle ScholarPubMed
58.Whitehouse, PJ.Parkinson’s diseases and Alzheimer’s disease: new neurochemical parallels. Movement Disorders 1989; 4 (Suppl 1): 57–62.CrossRefGoogle ScholarPubMed
59.Garofalo, O, Kennedy, PGE, Swash, M, et al. Ubiquitin and heat shock protein expression in amyotrophic lateral sclerosis. Neuropathol Appl Neurobiol 1991; 17: 39–45.CrossRefGoogle ScholarPubMed
60.Dale, GE, Leigh, PN, Luthert, P, et al. Neurofibrillary tangles in dementia pugilistica are unbiquinated. J Neurol Neurosurg Psychiatry 1991; 54: 116–118.CrossRefGoogle Scholar
61.Leigh, PN, Anderton, BH, Dodson, A, et al. Ubiquitin deposits in anterior horn cells in motor neuron disease. Neurosci Lett 1988; 93: 197–203.CrossRefGoogle Scholar
62.Murayama, S, Mori, H, Ihara, Y, et al. Immunocytochemical and ultrastructural studies of lower motor neurons in amyotrophic lateral sclerosis. Ann Neurol 1990; 27: 137–148.CrossRefGoogle ScholarPubMed
63.Drachman, DB, Kuncl, RW.Amyotrophic lateral sclerosis: an unconventional autoimmune disease? Ann Neurol 1989; 26: 269–274.CrossRefGoogle ScholarPubMed
64.McGeer, PL, ltagaki, S, Tago, H, et al. Reactive microglia in patients with senile dementia of the Alzheimer’s type are positive for the histocompatibility glycoprotein HLA-DR. Neurosci Lett 1987; 79: 195–200.CrossRefGoogle ScholarPubMed
65.McGeer, PL, ltagaki, S, McGeer, EG.Expression of the histocompatibility glycoprotein HLA-DR in neurological disease. Acta Neuropathol 1988; 76: 550–557.CrossRefGoogle ScholarPubMed
66.Sobel, RA, Ames, MB.Major histocompatibility complex molecule expression in the human central nervous system: immunohisto-chemical analysis of 40 patients. J Neuropathol Exp Neurol 1988; 47: 19–28.CrossRefGoogle Scholar
67.Lampson, LA, Kushner, PK, Sobel, RA.Major histocompatibility complex antigen expression in the affected tissues in amyotrophic lateral sclerosis. Ann Neurol 1990; 28: 365–372.CrossRefGoogle ScholarPubMed
68.Moss, MB, Saint-Hilaire, M, Feldman, RG, et al. Spontaneously occurring Parkinson’s disease in a nonhuman primate. Ann Neurol 1991; 30: 297.Google Scholar
69.Eisen, A, Kim, S, Pant, B.Amyotrophic lateral sclerosis (ALS): a phylogenelic disease of the corticomotoneuron? Muscle & Nerve (in press).Google Scholar
70.Plaitakas, A, Constantakakis, E, Smith, J.The neuroexcitotoxic amino acids glutamate and aspartate are altered in spinal cords and brain in amyotrophic lateral sclerosis. Ann Neurol 1988; 24: 446–449.CrossRefGoogle Scholar
71.Plaitakis, A.Glutamate dysfunction and selective motor neuron degeneration in amyotrophic lateral sclerosis: a hypothesis. Ann Neurol 1990; 28: 3–8.CrossRefGoogle ScholarPubMed
72.Stone, TW, Burton, NR.NMDA receptors and ligands in the vertebrate CNS. Prog Neurobiol 1988; 30: 333–368.CrossRefGoogle ScholarPubMed
73.McDonald, JW, Johnston, MV.Physiological and pathophysiological roles of excitatory amino acids during central nervous system development. Brain Res Rev 1990; 15: 41–70.CrossRefGoogle ScholarPubMed
74.Young, AB, Penney, JB, Dauth, GW, et al. Glutamate or aspartate as a possible neurotransmitter of cerebral corticofugal fibres in the monkey. Neurology 1983; 33: 1513–1516.CrossRefGoogle ScholarPubMed
75.Hyman, BT, Van Hoesen, GW, Damasio, AR, et al. Alzheimer’s disease: cell-specific pathology isolates the hippocampal formation. Science 1984; 225: 1168–1170.CrossRefGoogle ScholarPubMed
76.Hyman, BT, Van Hoesen, GW, Kromer, LJ, et al. Perforant pathway changes and the memory impairment of Alzheimer’s disease. Ann Neurol 1986; 20: 472–481.CrossRefGoogle ScholarPubMed
77.Margaros, WF, Greenamyre, JT, Penney, JB.Glutamate dysfunction in Alzheimer’s disease: a hypothesis. Trends Neurosci 1987; 10: 65–67.Google Scholar
78.Hyman, BT, Van Hoesen, GW, Damasio, AR.Alzheimer’s disease: glutamate depletion in the hippocampal perforant pathway zone. Ann Neurol 1987; 22: 37–40.CrossRefGoogle ScholarPubMed
79.Kowall, NW, Beal, MF.Glutamate-, glutaminase-, and taurine-immunoreactive neurons develop neurofibrillary tangles in Alzheimer’s disease. Ann Neurol 1991; 29: 162–167.CrossRefGoogle ScholarPubMed
80.Goldman-Rakic, PS, Selmon, LD.New frontiers in basal ganglia research. Trends Neurosci 1990; 13: 241–244.CrossRefGoogle ScholarPubMed
81.Rouzaire-Dubois, B, Scarnati, E.Pharmacological study of the cortical-induced excitation of subthalamic nucleus neurons in the rat: evidence for amino acids as putative transmitters. Neuroscience 1987; 21: 429–440.CrossRefGoogle Scholar
82.Smith, Y, Parent, A.Neurons of the subthalamic nucleus in primates display glutamate but not GABA immunoreactivity. Brain Res 1988; 453: 353–356.CrossRefGoogle Scholar
83.Cedarbaum, JM, Sheu, KFR, Harding, BJ, et al. Deficiency of glutamate dehydrogenase in postmortem brain samples from parkinsonian putamen. Ann Neurol 1990; 28: 111–112.CrossRefGoogle ScholarPubMed
84.Clow, DW, Jhamandas, KJ.Characterization of L-glutamate action on the release of endogeneous dopamine from the rat caudate-putamen. J Pharmacol Exp Ther 1989; 248: 722–278.Google ScholarPubMed
85.Sonsella, PK, Nicklas, WJ, Heikkila, RE.Role for excitatory amino acids in methamphetamine-induced nigrostriatal dopaminergic toxicity. Science 1989; 244: 398–400.CrossRefGoogle Scholar
86.Turski, L, Bressler, K, Rettig, K, et al. Protection of substantia nigra from MPP+ neurotoxicity by N-methyl-D-aspartate antagonists. Nature 1991; 349: 414–418.CrossRefGoogle ScholarPubMed
87.Klockgether, T, Turski, L.NMDA antagonists potentiate antiparkinsonian actions of L-dopa in monoamine-depleted rats. Ann Neurol 1990; 28: 539–546.CrossRefGoogle ScholarPubMed
88.Alexander, GE, Crutcher, MD.Functional architecture of basal ganglia circuits: neuronal substrates of parallel processing. Trends Neurosci 1990; 13: 266–271.CrossRefGoogle Scholar
89.Albin, RL, Young, AB, Penney, JP.The functional anatomy of basal ganglia disorders. Trends Neurosci 1989; 12: 366–375.CrossRefGoogle ScholarPubMed
90.Carrozza, DP, Ferraro, TN, Golden, GT, et al. Partial characterization of kainic acid-induced striatal dopamine release using in vivo microdialysis. Brain Res 1991; 543: 69–76.CrossRefGoogle ScholarPubMed