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Inicio Revista Colombiana de Psiquiatría Deterioro cognitivo, nivel educativo y ocupación en una población de una clín...
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Vol. 39. Núm. 2.
Páginas 347-361 (junio 2010)
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Vol. 39. Núm. 2.
Páginas 347-361 (junio 2010)
Artículos originales
Acceso a texto completo
Deterioro cognitivo, nivel educativo y ocupación en una población de una clínica de memoria*
Cognitive Impairment, Education and Occupation in a Memory Clinic Population
Visitas
1373
Mónica Sánchez Contreras1, Germán Alberto Moreno Gómez2,
Autor para correspondencia
gamo@telmex.net.co

Correspondencia: Germán Alberto Moreno Gómez, Epidemiología Clínica, Departamento de Medicina Comunitaria, Universidad Tecnológica de Pereira, La Julita, Pereira, Colombia
, Luis Hernando García Ortiz3
1 MSc, The Department of Biomedical and Pharmaceutical Sciences, University of Montana, Estados Unidos. Centro de Biología Molecular y Biotecnología, Universidad Tecnológica de Pereira. Pereira, Colombia
2 MSc en Epidemiología Clínica. Departamento de Medicina Comunitaria, Universidad Tecnológica de Pereira. Pereira, Colombia
3 Médico especialista en Medicina Interna y Geriatría, Departamento de Ciencias Clínicas, Universidad Tecnológica de Pereira. Pereira, Colombia
Este artículo ha recibido
Información del artículo
Resumen
Introducción

Factores sociodemográficos y genéticos se han relacionado con el desarrollo del deterioro cognitivo y la progresión a demencia.

Método

En este estudio se evaluaron características sociodemográficas junto con el genotipo de la apolipoproteína E (ApoE) en individuos mayores de 55 años de edad con deterioro cognitivo leve (DCL) y demencia tipo Alzheimer (DTA) atendidos en una clínica de la memoria.

Resultados

De los individuos que consultaron la clínica de la memoria en un período de cuatro años, 155 (36%) cumplieron los criterios de inclusión y se clasificaron en grupos diagnósticos de acuerdo con la cuarta edición revisada del Manual diagnóstico y estadístico de los trastornos mentales (DSM-IV-TR) y los criterios del National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA). Los individuos con DTA y DCL se dedicaron más a ocupaciones predominantemente manuales durante el transcurso de la vida que los individuos cognitivamente sanos (p=0,014). Un porcentaje alto de los individuos con DCL y cognitivamente sanos (43%) dejaron su ocupación principal o cambiaron a una predominantemente manual después del retiro laboral. No se encontraron otros factores asociados con el deterioro cognitivo, entre éstos polimorfismos en ApoE.

Conclusión

Estos resultados sustentan una relación entre la ocupación principal durante el transcurso de la vida y el desarrollo de deterioro cognitivo después de los 55 años.

Palabras clave:
trastornos cognitivos
educación
ocupación
apolipoproteínas E
Abstract
Introduction

Socio-demographic and genetic factors have been involved in the development of cognitive impairment and its progression to dementia.

Method

The present study evaluates socio-demographic characteristics and the ApoE genotype in individuals older than 55 years with mild cognitive impairment (MCI) and Alzheimer's disease (AD), attending a memory clinic.

Results

155 individuals (36%) out of the total population who attended the memory clinic in a four-year period met the inclusion criteria. The study population was classified in diagnostic groups according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) and to the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association (NICNCDS-ADRDA) criteria. More AD and MCI individuals worked in mainly manual occupations throughout their lifetime compared to cognitively unimpaired individuals (p=0.014). A high percentage of individuals with MCI and of cognitively unimpaired individuals (43%) left their primary occupation or changed it for a mainly manual occupation after their retirement. No other factors associated to the cognitive impairment, including ApoE genotype, were found.

Conclusion

These results support a correlation between the primary occupation during lifetime and the development of cognitive impairment in individuals older than 55 years.

Key words:
Cognitive disorders
education
occupation
apolipoproteins E
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Referencias
[1]
P Visser.
Mild cognitive impairment, Wiley, (2006),
[2]
American Psychiatric Association A.
Quick reference to the diagnostic criteria from DSMIV, American Psychiatric Association, (2000),
[3]
G Pradilla, B Vesga, GENECO León-Sarmiento F; grupo.
Estudio neuroepidemiológico nacional (EPINEURO) colombiano.
Rev Panam Salud Publica, 14 (2003), pp. 104-111
[4]
World Health Organization.
The global burden of disease: 2004 update, WHO, (2008),
[5]
R Petersen.
Mild cognitive impairment: Transition from aging to Alzheimer's disease.
Alzheimer's disease: advances in etiology pathogenesis and therapeutics, pp. 141-152
[6]
G Bartzokis, P Lu, D Geschwind, N Edwards, J Mintz, J Cummings.
Apolipoprotein E genotype and age-related myelin breakdown in healthy individuals: implications for cognitive decline and dementia.
Arch Gen Psychiatry, 63 (2006), pp. 63-72
[7]
S Herukka, M Hallikainen, H Soininen, T Pirttilä.
CSF Abeta42 and tau or phosphorylated tau and prediction of progressive mild cognitive impairment.
[8]
CR Jack Jr, MM Shiung, SD Weigand, PC O'Brien, JL Gunter, BF Boeve, et al.
Brain atrophy rates predict subsequent clinical conversion in normal elderly and amnestic MCI.
[9]
Y Huang, K Weisgraber, L Mucke, RW Mahley.
Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease.
J Mol Neurosci, 23 (2004), pp. 189-204
[10]
J Poirier.
Apolipoprotein E and cholesterol metabolism in the pathogenesis and treatment of Alzheimer's disease.
Trends Mol Med, 9 (2003), pp. 94-101
[11]
CA Martins, A Oulhaj, CA de Jager, JH Williams.
APOE alleles predict the rate of cognitive decline in Alzheimer disease. A nonlinear model.
[12]
P Bretsky, JM Guralnik, L Launer, M Albert, TE Seeman, MacArthur Studies of Successful Aging.
The role of APOE-epsilon4 in longitudinal cognitive decline: MacArthur Studies of Successful Aging.
Neurology, 60 (2003), pp. 1077-1081
[13]
G Small, S Chen, S Komo, L Ercoli, S Bookheimer, K Miller, et al.
Memory self-appraisal in middle-aged and older adults with the apolipoprotein E-4 allele.
Am J Psychiatry, 156 (1999), pp. 1035-1038
[14]
R Caselli, E Reiman, D Osborne, J Hentz, L Baxter, J Hernandez, et al.
Longitudinal changes in cognition and behavior in asymptomatic carriers of the APOE e4 allele.
Neurology, 62 (2004), pp. 1990-1995
[15]
J Levy, J Bergeson, K Putnam, V Rosen, R Cohen, F Lalonde, et al.
Context-specific memory and apolipoprotein E (ApoE) epsilon 4: Cognitive evidence from the NIMH prospective study of risk for Alzheimer's disease.
J Int Neuropsychol Soc, 10 (2004), pp. 362-370
[16]
C Marra, A Bizzarro, A Daniele, L De Luca, M Ferraccioli, A Valenza, et al.
Apolipoprotein E epsilon4 allele differently affects the patterns of neuropsychological presentation in early-and late-onset Alzheimer's disease patients.
Dement Geriatr Cogn Disord, 18 (2004), pp. 125-131
[17]
RC Petersen, GE Smith, RJ Ivnik, EG Tangalos, DJ Schaid, SN Thibodeau, et al.
Apolipoprotein E status as a predictor of the development of Alzheimer's disease in memory-impaired individuals.
J Am Med Assoc, 273 (1995), pp. 1274-1278
[18]
M Dik, C Jonker, L Bouter, M Geerlings, G van Kamp, D Deeg.
APOE-epsilon4 is associated with memory decline in cognitively impaired elderly.
Neurology, 54 (2000), pp. 1492-1497
[19]
I Deary, M Whiteman, A Pattie, J Starr, C Hayward, A Wright, et al.
Cognitive change and the APOE epsilon 4 allele.
Nature, 418 (2002), pp. 932
[20]
G Jarvik, E Larson, K Goddard, W Kukull, G Schellenberg, E Wijsman.
Influence of apolipoprotein E genotype on the transmission of Alzheimer disease in a community-based sample.
Am J Hum Genet, 58 (1996), pp. 191-200
[21]
T Ngandu, E von Strauss, E Helkala, B Winblad, A Nissinen, J Tuomilehto, et al.
Education and dementia. What lies behind the association?.
[22]
KA Smyth, T Fritsch, TB Cook, MJ McClendon, CE Santillan, RP Friedland.
Worker functions and traits associated with occupations and the development of AD.
Neurology, 63 (2004), pp. 498-503
[23]
G McKahnn, D Drahman, M Folstein, R Katzman, D Price, E Stadlan.
Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA. Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's disease.
Neurology, 34 (1984), pp. 939-944
[24]
DANE.
Clasificación Internacional Uniforme de Ocupaciones Adaptada para Colombia 1988 CIUO-88. Bogotá: DANE; 1988 [citado 23 Enero 2010] [Internet];.
[25]
J Sambrock, DW Russell.
Molecular Cloning: A Laboratory Manual, 3rd ed., Cold Spring Harbor Laboratory, (2001),
[26]
J Hixon, D Vernier.
Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI.
J Lipid Res, 31 (1990), pp. 545-548
[27]
J Rodríguez, V Cediel.
Genotipificación de apolipoproteína E en la población de Risaralda.
Rev Med Risaralda, 5 (1999), pp. 2-7
[28]
N Scarmeas, Y Stern.
Cognitive reserve and lifestyle.
J Clin Exp Neuropsychol, 25 (2003), pp. 625-633
[29]
H Christensen, P Batterham, A Mackinnon, K Anstey, W Wen, P Sachdev.
Education, atrophy, and cognitive change in an epidemiological sample in early old age.
Am J Geriatr Psychiatry, 17 (2009), pp. 218-226
[30]
A Karp, R Andel, MG Parker, HX Wang, B Winblad, L Fratiglioni.
Mentally stimulating activities at work during Midlife and dementia risk after age 75: follow-up study from the Kungsholmen Project.
Am J Geriatr Psychiatry, 17 (2009), pp. 227-236
[31]
PS Sachdev, M Valenzuela.
Brain and cognitive reserve.
Am J Geriatr Psychiatry, 17 (2009), pp. 175-178
[32]
Y Stern, B Gurland, T Tatemichi, M Tang, D Wilder, R Mayeux.
Influence of education and occupation on the incidence of Alzheimer's disease.
JAMA, 271 (1994), pp. 1004-1010
[33]
C Helmer, L Letenneur, I Rouch, S Richard-Harston, P Barberger-Gateau, C Fabrigoule, et al.
Occupation during life and risk of dementia in French elderly community residents.
J Neurol Neurosurg Psychiatry, 71 (2001), pp. 303-309
[34]
T Anttila, E Helkala, M Kivipelto, M Hallikainen, K Alhainen, H Heinonen, et al.
Midlife income, occupation, APOE status, and dementia: A population-based study.
Neurology, 59 (2002), pp. 887-893
[35]
P Visser.
Medicine in old age.
Principles and practice of geriatric medicine, pp. 1-7
[36]
D Bartrés-Faz, J Serra-Grabulosa, F Sun, C Solé-Padullés, L Rami, J Molinuevo, et al.
Functional connectivity of the hippocampus in elderly with mild memory dysfunction carrying the APOE ¿4 allele.
Neurobiol Aging, 29 (2008), pp. 1644-1653
[37]
JC Hays, BM Burchett, GG Fillenbaum, DG Blazer.
Is the APOE □4 allele a risk to person-environment fit?.
J Appl Gerontol, 23 (2004), pp. 247-265
[38]
M Greicius, M Geschwind, B Miller.
Presenile dementia syndromes: an update on taxonomy and diagnosis.
J Neurol Neurosurg Psychiatry, 72 (2002), pp. 691-700
[39]
HA Keage, FE Matthews, A Yip, L Gao, C McCracken, IG McKeith, et al.
APOE and ACE polymorphisms and dementia risk in the older population over prolonged follow-up: 10 years of incidence in the MRC CFA Study.
Age and Ageing, 39 (2009), pp. 104-111
[40]
C Solé-Padullés, I Clemente, D Bartrés-Faz.
Marcadores genéticos relacionados con el déficit cognitivo en el envejecimiento.
Anales de Psicología, 20 (2004), pp. 187-204

Conflicto de interés: los autores manifiestan que no tienen ningún conflicto de interés en este artículo.

Este trabajo fue financiado por la Universidad Tecnológica de Pereira. Hace parte de la tesis de Maestría en Biología Molecular y Biotecnología, “Prevalencia de los polimorfismos del gen APOE en una población de ancianos de la ciudad de Pereira con deterioro cognitivo leve, enfermedad de Alzheimer y cognitivamente sanos”, 2007, Universidad Tecnológica de Pereira. Se presentó en el VI Seminario Internacional y V Encuentro Nacional de Neurociencias, Cali, Colombia, el 6 de octubre de 2006.

Copyright © 2010. Asociación Colombiana de Psiquiatría
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