Alterações encontradas em cérebros de indivíduos acima dos 65 anos e sua correlação com demência de Alzheimer

Fernandez, Liana Lisboa; Barbosa-Coutinho, Lígia M.

doi:10.1590/S0004-282X1997000200019

Resumos

Foram estudadas 12 amostras de cérebros de indivíduos acima de 65 anos. Estas amostras foram submetidas a três técnicas com o objetivo de se detectar placas senis ricas em β-amilóide: imuno-histoquímica para β-amilóide; técnica de Glees; técnica da hematoxilina-eosina. Foram detectadas diferenças significativas entre o número de placas encontradas nas diferentes técnicas, o que salienta a possibilidade de diagnósticos falsos-negativos na doença de Alzheimer. A técnica de imuno-histoquímica mostrou-se mais eficiente. Foram submetidos a teste estatístico o número de placas encontradas no cortex e no hipocampo e comparadas, assim como o número de placas encontradas num hemisfério e no outro, sem diferenças significativas. Segue-se revisão da literatura quanto aos achados neuropatológicos da doença de Alzheimer, assim como da significância do β-amilóide.

doença de Alzheimer; placas senis; β-amiloide

Twelve brains of individuals with more than sixty-five years were studied. These samples were submitted to three techniques, with the objective to detect senile plaques which the major component was the β-amyloid: -β -amyloid immunohistochemistry; Glees technique; and haematoxilin-eosin technique. We detected significant differences between the number of senile plaques found in different techniques. β-amyloid immunohistochemistry was more efficient. This is very important because we can underdiagnosis Alzheimer's disease when the most adequate technique is not used. The statistical analysis showed no significant differences neither between the number of cortical plaques and the hipocampal plaques,nor between the number of plaques in both hemispheres. A literature review about neuropathological findings and β-amyloid importance was done.

Alzheimer disease; senile plaques; β-amyloid

Alterações encontradas em cérebros de indivíduos acima dos 65 anos e sua correlação com demência de Alzheimer

Changes found in the brain of people over 65 years old and their correlation with Alzheimer disease

Liana Lisboa Fernandez^I; Lígia M. Barbosa-Coutinho^II

^IMédica neurologista; Professor titular de Anatomia Patológica da Fundação Faculdade Federal de Ciências Médicas de Porto Alegre (FFFCMPA)

^IINeuropatologista, Professor titular de Anatomia Patológica da Fundação Faculdade Federal de Ciências Médicas de Porto Alegre (FFFCMPA)

RESUMO

Foram estudadas 12 amostras de cérebros de indivíduos acima de 65 anos. Estas amostras foram submetidas a três técnicas com o objetivo de se detectar placas senis ricas em β-amilóide: imuno-histoquímica para β-amilóide; técnica de Glees; técnica da hematoxilina-eosina. Foram detectadas diferenças significativas entre o número de placas encontradas nas diferentes técnicas, o que salienta a possibilidade de diagnósticos falsos-negativos na doença de Alzheimer. A técnica de imuno-histoquímica mostrou-se mais eficiente. Foram submetidos a teste estatístico o número de placas encontradas no cortex e no hipocampo e comparadas, assim como o número de placas encontradas num hemisfério e no outro, sem diferenças significativas. Segue-se revisão da literatura quanto aos achados neuropatológicos da doença de Alzheimer, assim como da significância do β-amilóide.

Palavras-chave: doença de Alzheimer, placas senis, β-amiloide.

ABSTRACT

Twelve brains of individuals with more than sixty-five years were studied. These samples were submitted to three techniques, with the objective to detect senile plaques which the major component was the β-amyloid: -β -amyloid immunohistochemistry; Glees technique; and haematoxilin-eosin technique. We detected significant differences between the number of senile plaques found in different techniques. β-amyloid immunohistochemistry was more efficient. This is very important because we can underdiagnosis Alzheimer's disease when the most adequate technique is not used. The statistical analysis showed no significant differences neither between the number of cortical plaques and the hipocampal plaques,nor between the number of plaques in both hemispheres. A literature review about neuropathological findings and β-amyloid importance was done.

Key words: Alzheimer disease, senile plaques, β-amyloid.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Aceite: 24-janeiro-1997.

Dra. Liana Lisboa Fernandez - Rua Cel. Bordini 675/204 - 90440-001 Porto Alegre RS - Brasil.

1. Almeida OP, Nitrini R (eds). Demência. São Paulo: Bik 1995:13-136.
2. Alzheimer A. Übereineeigenartige Erkwankung der Hirnrindel. Allg A PsychiatPsych Gerictl Med 1907;64:146-148.
3. Blom N, Linnemann D. Alzheimer's dementia and amyloid precursor-protein. Ugestr-Laeger (Denmark) 1992; 154:1010-1015.
4. Cotman CW, Pike CJ. Beta-amyloid and its contributions to neurodegenerations in Alzheimer disease. In Terry RD, Katzman R., Bick KL (eds). Alzheimer disease. New York: Raven Press, 1994:305-315.
5. Davies P. Neuronal abnormalities, not amyloid, are the cause of dementia in Alzheimer disease. In Terry RD, Katzman R., Bick KL (eds). Alzheimer disease. New York; Raven Press 1994:327-333.
6. Fernandez RJ, Samuels MA. Disfunção intelectual: retardo mental e demência. Manual de neurologia. Rio de Janeiro: Medsi 1992:41-43.
7. Golaz J, Boures C, Hof PR. Motor cortex involvement in presenile dementia: report of a case. J Geriatr Psychiatry Neurol 1992;5:85-92.
8. Goldgaber D; Schmechel DE. Expression of the amyloid beta-protein precursor gene. In Wurtman RJ et al. (eds). Advances in neurology: Alzheimer disease. New York: Raven Press 1990,51.
9. Haass C_T Hung AY, Citron M, Teplow DB, Selkoe DJ. Beta-amyloid, protein processing and Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:398-402.
10. Hardy J. An anatomical cascade hypothesis for Alzheimer's disease. TINS 1992;15:200-201.
11. Hauw JJ. Duyckaerts C, Delaere P. Alzheimer's disease. In Duckett S (ed). The pathology of the aging human nervous system.Philadelphia: Lea&Febiger, 1991:113-147.
12. Hof PR. Perl DP. Loerzel AJ, Morrison JH. Neurofibrillary tangle: distribution in the cerebral cortex of parkinsonism dementia cases from Guam: differences with Alzheimer disease. Brain Res (Netherlands) 1991,564:306-313.
13. Ince P, Irving D, Macartur F, Perry RH. Quantitative neuropathological study of Alzheimer-type pathology in the hyppocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson's disease and non-demented elderly control patients. Neurol Sci (Netherlands) 1991 ;106:42-52.
14. Jarret JT, Berger EP, Lansbury PT. Carboxyterminus of beta-amyloid protein is critical for seeding of amyloid formation: implicatons for the pathogenesis of Alzheimer's disease. J Biochem 1993;32:4693-4697.
15. Joachim CL, Selkoe DJ. The potential role of beta-amyloid in the pathogenesis of Alzheimer disease. Alzheimer Dis Assoc Disord 1992;6:7-34.
16. Kemper RL. Neuroanatomical and neuropathological changes during aging and dementia. In Albert ML, Knoefel JE. (eds). Clinical neurology of aging. New York: Oxford Univ Press, 1994:3-67.
17. Koukolik F. Relation of dementia, Alzheimer's disease and aging. Oddeleni patologie, Fakulthi Tomayerovy Nemocnice, Praha, Ceskpat (Czechoslovakia) 1992;28:14-20.
18. Lansbury PTJr. Consequences of the molecular mechanism of amyloid formation forthe understanding of the pathogenesis of Alzheimer's disease and the development of therapeutic strategies. Arzneimittel Forschung Drug Res 1995,45:432-434.
19. Masters CL, Beyreuther K. Molecular neuropathology of Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:410-412.
20. Masters CL, Beyreuther K. Protein abnormalities in neurofibrillary tangles: their relation to the extracellular amyloid deposits of the A4 protein in Alzheimer's disease. In Wintman Ret al. (eds). Advances in neurology. New York: Raven Press 1990,51:151-161.
21. Maury CPJ. Molecular pathogenesis of beta-amyloid in Alzheimer's disease and other cerebral amyloidoses. Laborat Invest 1995;71:4-16.
²²
Merrill's text book of neurology. Ed. 7 Rowland LP (ed). Philadelphia: Lea & Febinger, 1994:508-514.
23. Nitsch RM, Wurtman RJ, Growdon JH. Regulation of proteolytic processing of the amyloid beta-protein precursor by first messengers: a novel potential approach for the treatment of Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:435-438.
24. Robakis NK. Beta-amyloid and amyloid precursor protein chemistry molecular biology and neuropathology. In Terry RD, Katzman R, BickKL(eds). Alzheimerdisea.se. New York: Raven Press, 1994:317-326.
25. Schorderet M. Alzheimer's disease: fundamental and therapeutic aspects. Experientia 1995,51:99-105.
26. Sisodia SS. Price DL. Role of the beta-amyloid protein in Alzheimer's disease. FASEB 1995,9:366-370.
27. Strittmatter WJ, Apel SM. Alzheimer's disease.Curr Neurol 1990;10:357-379.
28. Strittmatter WJ, Roses AD. Apolipoprotein E and Alzheimer disease. Proc Natl Acad Sci USA 1995,92:4725-4727.
29. Van Broeckhoven CL. Molecular genetics of Alzheimer disease: identification of genes and gene mutations. Eur Neurol 1995; 35:8-19.

Datas de Publicação

Publicação nesta coleção
10 Nov 2010
Data do Fascículo
Jun 1997

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Almeida OP, Nitrini R (eds). Demência. São Paulo: Bik 1995:13-136.

[2] 2. Alzheimer A. Übereineeigenartige Erkwankung der Hirnrindel. Allg A PsychiatPsych Gerictl Med 1907;64:146-148.

[3] 3. Blom N, Linnemann D. Alzheimer's dementia and amyloid precursor-protein. Ugestr-Laeger (Denmark) 1992; 154:1010-1015.

[4] 4. Cotman CW, Pike CJ. Beta-amyloid and its contributions to neurodegenerations in Alzheimer disease. In Terry RD, Katzman R., Bick KL (eds). Alzheimer disease. New York: Raven Press, 1994:305-315.

[5] 5. Davies P. Neuronal abnormalities, not amyloid, are the cause of dementia in Alzheimer disease. In Terry RD, Katzman R., Bick KL (eds). Alzheimer disease. New York; Raven Press 1994:327-333.

[6] 6. Fernandez RJ, Samuels MA. Disfunção intelectual: retardo mental e demência. Manual de neurologia. Rio de Janeiro: Medsi 1992:41-43.

[7] 7. Golaz J, Boures C, Hof PR. Motor cortex involvement in presenile dementia: report of a case. J Geriatr Psychiatry Neurol 1992;5:85-92.

[8] 8. Goldgaber D; Schmechel DE. Expression of the amyloid beta-protein precursor gene. In Wurtman RJ et al. (eds). Advances in neurology: Alzheimer disease. New York: Raven Press 1990,51.

[9] 9. Haass C_T Hung AY, Citron M, Teplow DB, Selkoe DJ. Beta-amyloid, protein processing and Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:398-402.

[10] 10. Hardy J. An anatomical cascade hypothesis for Alzheimer's disease. TINS 1992;15:200-201.

[11] 11. Hauw JJ. Duyckaerts C, Delaere P. Alzheimer's disease. In Duckett S (ed). The pathology of the aging human nervous system.Philadelphia: Lea&Febiger, 1991:113-147.

[12] 12. Hof PR. Perl DP. Loerzel AJ, Morrison JH. Neurofibrillary tangle: distribution in the cerebral cortex of parkinsonism dementia cases from Guam: differences with Alzheimer disease. Brain Res (Netherlands) 1991,564:306-313.

[13] 13. Ince P, Irving D, Macartur F, Perry RH. Quantitative neuropathological study of Alzheimer-type pathology in the hyppocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson's disease and non-demented elderly control patients. Neurol Sci (Netherlands) 1991 ;106:42-52.

[14] 14. Jarret JT, Berger EP, Lansbury PT. Carboxyterminus of beta-amyloid protein is critical for seeding of amyloid formation: implicatons for the pathogenesis of Alzheimer's disease. J Biochem 1993;32:4693-4697.

[15] 15. Joachim CL, Selkoe DJ. The potential role of beta-amyloid in the pathogenesis of Alzheimer disease. Alzheimer Dis Assoc Disord 1992;6:7-34.

[16] 16. Kemper RL. Neuroanatomical and neuropathological changes during aging and dementia. In Albert ML, Knoefel JE. (eds). Clinical neurology of aging. New York: Oxford Univ Press, 1994:3-67.

[17] 17. Koukolik F. Relation of dementia, Alzheimer's disease and aging. Oddeleni patologie, Fakulthi Tomayerovy Nemocnice, Praha, Ceskpat (Czechoslovakia) 1992;28:14-20.

[18] 18. Lansbury PTJr. Consequences of the molecular mechanism of amyloid formation forthe understanding of the pathogenesis of Alzheimer's disease and the development of therapeutic strategies. Arzneimittel Forschung Drug Res 1995,45:432-434.

[19] 19. Masters CL, Beyreuther K. Molecular neuropathology of Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:410-412.

[20] 20. Masters CL, Beyreuther K. Protein abnormalities in neurofibrillary tangles: their relation to the extracellular amyloid deposits of the A4 protein in Alzheimer's disease. In Wintman Ret al. (eds). Advances in neurology. New York: Raven Press 1990,51:151-161.

[21] 21. Maury CPJ. Molecular pathogenesis of beta-amyloid in Alzheimer's disease and other cerebral amyloidoses. Laborat Invest 1995;71:4-16.

[22] ²²
Merrill's text book of neurology. Ed. 7 Rowland LP (ed). Philadelphia: Lea & Febinger, 1994:508-514.

[23] 23. Nitsch RM, Wurtman RJ, Growdon JH. Regulation of proteolytic processing of the amyloid beta-protein precursor by first messengers: a novel potential approach for the treatment of Alzheimer's disease. Arzneimittel Forschung Drug Res 1995;45:435-438.

[24] 24. Robakis NK. Beta-amyloid and amyloid precursor protein chemistry molecular biology and neuropathology. In Terry RD, Katzman R, BickKL(eds). Alzheimerdisea.se. New York: Raven Press, 1994:317-326.

[25] 25. Schorderet M. Alzheimer's disease: fundamental and therapeutic aspects. Experientia 1995,51:99-105.

[26] 26. Sisodia SS. Price DL. Role of the beta-amyloid protein in Alzheimer's disease. FASEB 1995,9:366-370.

[27] 27. Strittmatter WJ, Apel SM. Alzheimer's disease.Curr Neurol 1990;10:357-379.

[28] 28. Strittmatter WJ, Roses AD. Apolipoprotein E and Alzheimer disease. Proc Natl Acad Sci USA 1995,92:4725-4727.

[29] 29. Van Broeckhoven CL. Molecular genetics of Alzheimer disease: identification of genes and gene mutations. Eur Neurol 1995; 35:8-19.