CC BY 4.0 · Arq Neuropsiquiatr 2023; 81(12): 1070-1076
DOI: 10.1055/s-0043-1777722
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The past, present and future of Alzheimer's disease – part 1: the past

O passado, presente e futuro da doença de Alzheimer – parte 1: o passado
1   Universidade de São Paulo, Faculdade de Medicina, São Paulo SP, Brazil.
› Author Affiliations

Abstract

Background Alzheimer's disease (AD) was described in 1907, and since then it changed from a relatively rare condition to one of the most prevalent diseases.

Objective To describe the evolution of the notions of dementias and AD, and to investigate the reasons for the increase in scientific interest in AD.

Methods A historical analysis was carried out on knowledge about dementia, the site of mental activity, the relationships between brain diseases and mental activity, and on the advances in research about AD, since its discovery until the publication of the amyloid cascade hypothesis in 1992. A search was carried out in the National Library of Medicine (PubMed) for scientific articles that included the terms dementia or AD over 50 years, from 1972 to 2021.

Results The scientific research on AD increased from 615 papers with the term AD in the first decade (1972-1981), to 100,028 papers in the last decade (2012-2021): an increase of 162.6 times whereas publications with the term dementia increased 28.6 times in the same period. In the 1960s and 1970s, a consensus was reached that AD is responsible for the majority of cases of dementia previously known as senile dementia. In the 1980s, beta-amyloid peptide was identified in the core of the senile plaque, hyperphosphorylated tau protein was found in neurofibrillary tangles, and a mutation was discovered in a hereditary form of AD.

Conclusion The expansion of the concept of AD to include senile dementia, and the discoveries that occurred in the 1980s greatly expanded research in AD.

Resumo

Antecedentes A doença de Alzheimer (DA) foi descrita em 1907 e, desde então, deixou de ser relativamente rara para se tornar uma das doenças mais prevalentes.

Objetivo Descrever a evolução das noções sobre demências e DA e investigar as razões do aumento do interesse científico pela DA.

Métodos Foi realizada uma análise histórica dos conhecimentos sobre demência, o local da atividade mental, as relações entre doenças cerebrais e a atividade mental, e sobre os avanços na pesquisa sobre a DA, desde a sua descoberta até a publicação da hipótese da cascata amiloide em 1992. Foi realizada uma busca na Biblioteca Nacional de Medicina dos Estados Unidos da América (PubMed) por artigos científicos que incluíssem os termos demência ou DA nos 50 anos, de 1972 a 2021.

Resultados A pesquisa científica sobre DA aumentou de 615 artigos com o termo doença de Alzheimer na primeira década (1972-1981), para 100.028 artigos na última década (2012-2021): um aumento de 162,6 vezes enquanto as publicações com o termo demência aumentaram 28,6 vezes no mesmo período. Nas décadas de 1960 e 1970, chegou-se a um consenso de que a DA é responsável pela maioria dos casos de demência, anteriormente conhecida como demência senil. Na década de 1980, o peptídeo beta-amiloide foi identificado no núcleo da placa senil, a proteína tau hiperfosforilada foi encontrada em emaranhados neurofibrilares e uma mutação foi descoberta em uma forma hereditária de DA.

Conclusão A expansão do conceito de DA para incluir a demência senil e as descobertas ocorridas na década de 1980 ampliaram enormemente a pesquisa em DA.



Publication History

Received: 10 October 2023

Accepted: 21 November 2023

Article published online:
29 December 2023

© 2023. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution 4.0 International License, permitting copying and reproduction so long as the original work is given appropriate credit (https://creativecommons.org/licenses/by/4.0/)

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  • References

  • 1 Karenberg A, Förstl H. Dementia in the Greco-Roman world. J Neurol Sci 2006; 244 (1-2): 5-9
  • 2 Cicero MT. Cato Maior De Senectude. New York: Cambridge University Press;; 1988
  • 3 Gross CG. Aristotle on the brain. Neuroscientist 1995; 1: 245-250
  • 4 Quétel C. History of Syphilis. Baltimore:: Johns Hopkins University Press;; 1990: 160-161 .(Translated from the 1986 French edition)
  • 5 Kraepelin E. One hundred years of psychiatry. New York: Philosophical Library; 1962. (Translated from the 1917 German edition.) p. 130
  • 6 Nitrini R. The cure of one of the most frequent types of dementia: a historical parallel. Alzheimer Dis Assoc Disord 2005; 19 (03) 156-158
  • 7 Maurer K, Maurer U. Alzheimer: the life of a physician and the career of a disease. New York: Columbia University Press; 2003. (Translated from the 1998 German edition.)
  • 8 Alzheimer A. A characteristic disease of the cerebral cortex. Allgemeine Zeitschrift für Psychiatrie un Psychisch-Gerichtliche Medizin,. 1907; 64:146-148. In: Bick K, Amaducci L, Pepeu G. eds. The Early Story of Alzheimer's Disease. Padova: Liviana Press; 1987: 1-3
  • 9 Isler R. Neurology and the neurological sciences in the German-speaking countries. In: Finger S, Boller F, Tyler KL. eds. History of neurology. Handbook of clinical neurology; 2010. ;95: 667-689
  • 10 Nitrini R. [Neurology as a medical specialty: a historic interpretation] In Portuguese. A Neurologia como Especialidade Médica: Uma Interpretação Histórica. In: Gagliardi R. , Takayanagui, eds. Tratado de Neurologia da Academia Brasileira de Neurologia. 2ª ed,. Rio de Janeiro: Elsevier; 2019: 12-16
  • 11 Merritt HH, Adams RD, Solomon HC. Neurosyphilis. New York: Oxford University Press; 1946: 176
  • 12 Hippius H, Neundörfer G. The discovery of Alzheimer's disease. Dialogues Clin Neurosci 2003; 5 (01) 101-108
  • 13 Pérez-Trullén JM. A brief biography of Alois Alzheimer. Neurosci Hist 2013; 1 (03) 125-136
  • 14 Gomes MDM. Franz Nissl (1860-1919), noted neuropsychiatrist and neuropathologist, staining the neuron, but not limiting it. Dement Neuropsychol 2019; 13 (03) 352-355
  • 15 Teive HAG, Tensini FS, Lima PG, Camargo CHF. Constantin von Economós 90th death anniversary. Arq Neuropsiquiatr 2021; 79 (11) 1039-1042
  • 16 Pepeu G. Introduction. In In: Bick K, Amaducci L, Pepeu G. eds. The Early Story of Alzheimer's Disease. Padova: Liviana Press; 1987
  • 17 Neubuerger KT. The history of neuropathology. In: Minckler J. ed. The Pathology of the Nervous System. New York: McGraw-Hill Book Company; 1968: 1-14
  • 18 Kraepelin E. Senile and Pre-Senile Dementias. In: Bick K, Amaducci L, Pepeu G. eds. The Early Story of Alzheimer's Disease. Padova: Liviana Press; 1987: 32-81 , p. 77 (Translated from the 1910 German edition of Ein Lehrbuch für Studierende und Ärzte)
  • 19 Luria AR. The Working Brain: An Introduction to Neuropsychology. London: Penguin Books; 1973
  • 20 Luria AR. Higher Cortical Functions in Man. New York:: Basic Books; 1973
  • 21 Geschwind N. Disconnexion syndromes in animals and man. I. Brain 1965; 88 (02) 237-294
  • 22 Geschwind N. Disconnexion syndromes in animals and man. II. Brain 1965; 88 (03) 585-644
  • 23 Lefèvre BH, Nitrini R. [Neuropsychological semiology]. Arq Neuropsiquiatr 1985; 43 (02) 119-132 . Portuguese. Doi: 10.1590/s0004-282. Doi:  × 1985000200001. PMID: 4062596
  • 24 Mesulam M-M. Principles of Behavioral and Cognitive Neurology. Philadelphia: Davis; 1985
  • 25 Mesulam M-M. Principles of Behavioral and Cognitive Neurology. 2nd ed. New York: Oxford Universuty Press; 2000
  • 26 Mesulam MM, Rogalski EJ, Wieneke C. et al. Primary progressive aphasia and the evolving neurology of the language network. Nat Rev Neurol 2014; 10 (10) 554-569
  • 27 Miller B, Llibre Guerra JJ. Frontotemporal dementia. Handb Clin Neurol 2019; 165: 33-45
  • 28 Grossman M, Seeley WW, Boxer AL. et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers 2023; 9 (01) 40
  • 29 Nitrini R. Elementary motor perseveration in early diagnosis of progressive supranuclear palsy. Arq Neuropsiquiatr 1987; 45 (01) 29-32 . Doi: 10.1590/s0004-282. Doi:  × 1987000100004
  • 30 Dubois B, Slachevsky A, Pillon B, Beato R, Villalponda JM, Litvan I. “Applause sign” helps to discriminate PSP from FTD and PD. Neurology 2005; 64 (12) 2132-2133
  • 31 Delay J, Brion S. Les Démences Tardives. Paris:: Masson; 1962
  • 32 Newton RD. The identity of Alzheimer's disease and sinile dementia and their relationship to senility. J Ment Sci 1948; 94 (395) 225-249
  • 33 Neumann MA, Cohn R. Incidence of Alzheimer's disease in large mental hospital; relation to senile psychosis and psychosis with cerebral arteriosclerosis. AMA Arch Neurol Psychiatry 1953; 69 (05) 615-636
  • 34 Roth M, Tomlinson BE, Blessed G. Correlation between scores for dementia and counts of 'senile plaques' in cerebral grey matter of elderly subjects. Nature 1966; 209 (5018) 109-110
  • 35 Hachinski VC, Lassen NA, Marshall J. Multi-infarct dementia. A cause of mental deterioration in the elderly. Lancet 1974; 2 (7874) 207-210
  • 36 Katzman R. The prevalence and malignancy of Alzheimer disease: a major killer. Alzheimers Dement 2008; 4 (06) 378-380
  • 37 Goedert M. Oskar Fischer and the study of dementia. Brain 2009; 132 (Pt 4(: 1102-1111
  • 38 Amaducci LA, Rocca WA, Schoenberg BS. Origin of the distinction between Alzheimer's disease and senile dementia: how history can clarify nosology. Neurology 1986; 36 (11) 1497-1499
  • 39 Fischer O. Miliary necrosis with nodular proliferation of the neurofibrils, a common change of the cerebral cortex in senile dementia. Monatsschrift für Psychiatrie und Neurologie. 2007. ;22:361-372. In Bick K, Amaducci L, Pepeu G. eds. The Early Story of Alzheimer's Disease. Padova: Liviana Press; 1987: 5-18
  • 40 Allsop D, Landon M, Kidd M. The isolation and amino acid composition of senile plaque core protein. Brain Res 1983; 259 (02) 348-352
  • 41 Glenner GG, Wong CW. Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun 1984; 120 (03) 885-890
  • 42 Glenner GG, Wong CW. Alzheimer's disease and Down's syndrome: sharing of a unique cerebrovascular amyloid fibril protein. Biochem Biophys Res Commun 1984; 122 (03) 1131-1135
  • 43 Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci U S A 1985; 82 (12) 4245-4249 . PMID: 3159021; PMCID: PMC397973.Allsop et al., 1983;
  • 44 St George-Hyslop PH, Tanzi RE, Polinsky RJ. et al. The genetic defect causing familial Alzheimer's disease maps on chromosome 21. Science 1987; 235 (4791) 885-890
  • 45 Grundke-Iqbal I, Iqbal K, Quinlan M, Tung YC, Zaidi MS, Wisniewski HM. Microtubule-associated protein tau. A component of Alzheimer paired helical filaments. J Biol Chem 1986; 261 (13) 6084-6089
  • 46 Grundke-Iqbal I, Iqbal K, Tung YC, Quinlan M, Wisniewski HM, Binder LI. Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology. Proc Natl Acad Sci U S A 1986; 83 (13) 4913-4917
  • 47 Terry RD, Davies P. Dementia of the Alzheimer type. Annu Rev Neurosci 1980; 3: 77-95
  • 48 Selkoe DJ. Aging, amyloid, and Alzheimer's disease. N Engl J Med 1989; 320 (22) 1484-1487
  • 49 de Paula VJR, Guimarães FM, Diniz BS, Forlenza OV. Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?. Dement Neuropsychol 2009; 3 (03) 188-194
  • 50 Hardy JA, Higgins GA. Alzheimer's disease: the amyloid cascade hypothesis. Science 1992; 256 (5054) 184-185