Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?

44 Páginas.

Autores:
Rugeles Castañeda, Andrea
Tipo de recurso:
Fecha de publicación:
2007
Institución:
Universidad de la Sabana
Repositorio:
Repositorio Universidad de la Sabana
Idioma:
spa
OAI Identifier:
oai:intellectum.unisabana.edu.co:10818/2168
Acceso en línea:
http://hdl.handle.net/10818/2168
Palabra clave:
Enfermedad de Alzheimer
Enfermedades del sistema nervioso
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License
http://purl.org/coar/access_right/c_abf2
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network_name_str Repositorio Universidad de la Sabana
repository_id_str
dc.title.es_CO.fl_str_mv Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
title Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
spellingShingle Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
Enfermedad de Alzheimer
Enfermedades del sistema nervioso
title_short Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
title_full Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
title_fullStr Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
title_full_unstemmed Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
title_sort Alzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?
dc.creator.fl_str_mv Rugeles Castañeda, Andrea
dc.contributor.advisor.none.fl_str_mv Suárez Baquero, Alejandra
dc.contributor.author.none.fl_str_mv Rugeles Castañeda, Andrea
dc.subject.es_CO.fl_str_mv Enfermedad de Alzheimer
Enfermedades del sistema nervioso
topic Enfermedad de Alzheimer
Enfermedades del sistema nervioso
description 44 Páginas.
publishDate 2007
dc.date.created.none.fl_str_mv 2007
dc.date.accessioned.none.fl_str_mv 2012-05-15T19:16:46Z
dc.date.available.none.fl_str_mv 2012-05-15T19:16:46Z
dc.date.issued.none.fl_str_mv 2012-05-15
dc.type.none.fl_str_mv bachelorThesis
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dc.type.coar.fl_str_mv http://purl.org/coar/resource_type/c_7a1f
dc.type.local.none.fl_str_mv Tesis de pregrado
dc.type.hasVersion.none.fl_str_mv publishedVersion
dc.identifier.citation.none.fl_str_mv Algado, M.T., et al.(1997). Familia y enfermedad de Alzheimer.Una perspectiva cualitativa. Anales de Psicología, (13), p.21.
Bartus, RT.(2000) On neurodegenerative diseases, models, and treatment strategies:lessons learned and lessons forgotten a generation following the cholinergic hupothesis. Exp Neurol (163).
Bermejo, FP. (1998) La enfermedad de Alzheimer. Medicina Interna (16).
Blasco, I. & Grubeck-Loebenstein, B.(2003). Role of the immune system in the pathogenesis, prevention and treatment of Alzheimer’s disease. Drugs Aging.(20).p.105.
Blasco, I. et al.(2004). How chronic inflammation affects the brain and supports the development of Alzheimer’s disease in old age: the role of microglia and astrocytes. Aging Cell.(3).
Buffil, E. & Blesa, R. (2006) Alzheimer’s Disease And Brain Evolution: Is Alzheimer's Disease An Example Of Antagonistic Pleiotropy?. Revista de Neurología (42).pp.25-26
Campion, D. et al.(1999). Early-onset autosomal dominant Alzheimer disease: prevalence,genetic heterogeneity, and mutation spectrum. American Journal Hum Genet.(65).p.668.
Cruts, M. & Van Broeckhoven, C.(1998).Presenilin mutations in Alzheimer’s disease.Hum Mutat. (11).
Farrer, LA. et al.(1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis.
APOE and Alzheimer Disease Meta Analysis Consortium. JAMA.(278).p.1350.
Flynn, DD. Et al.(1995). Differential alterations in muscarinic receptor subtypes in Alzheimer’s disease: implications for cholinergicbased therapies. Life Sci (56).p.86.
Forstl, H. et al. (1992).Clinical and neuropathological correlatesof depression in Alzheimer’s disease. Psychol Med.(22).
Gálvez, R. et al. (2000) Epidemiología de la enfermedades degenerativas del sistema nervioso. Barcelona: ed. Masson Salvat-Medicina.
Gómez,T. et al.(1997).Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer’s disease. Ann Neurol. (41).p.19
Gottfries, CG. et al.(1995) Neuropeptides and Alzheimer’s disease. Eur Neuropsychopharmacol.(5).
Hardy, J.et al.(1998).Genetic dissection of Alzheimer’s disease and related dementias: amyloid and its relationship to tau. Nat Neurosci. (1).p.371. Hoenicka, J. (2006) Genes In Alzheimer’s Disease.Rev Neurol.(42).pp.302-303
Huse, JT. & Doms, RW. (2000). Closing in on the amyloid cascade: recent insights into the cell biology of Alzheimer’s disease. Mol Neurobiol. (22).p.88.
Ikonomovic, MD.et al.(1999). Distribution of glutamate receptor subunit NMDAR1 in the hippocampus of normal elderly and patients with Alzheimer’s disease. Exp Neurol.(160)
Kordower, JH. Et al. (2001). Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment. Ann Neurol (49).
Lanctot, KL. et al (2001) Role of serotonin in the behavioraland psychological symptoms of dementia. Journal of Neuropsychiat Clinical. (13).p.521.
Lewis, J. et al.(2001) Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science. (293).
Li, YM. et al.(2000).Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1. Nature.(405)
López, L. & DeKosky, S. (2003). Neuropatología de la enfermedad de Alzheimer y del deterioro cognitivo leve. Revista Neurologica. (37).p158-159.
Maelicke, A. et al.(2000) Allosterically potentiating ligands of nicotinic receptors as a treatment strategy for Alzheimer’s disease. Behav Brain Res. (113).
Martín, CM.et al.(1999). Alpha4 but not Alpha3 and Alpha7 nicotinic acetylcholine receptor subunits are lost from the temporal cortex in Alzheimer’s disease. Journal Neurochem. (73).
Martin, JB.(1999). Molecular basis of the neurodegenerative disorders. New England Journal Med.(340).
Marutle, A, et al.(1999) Neuronal nicotinic receptor deficits in Alzheimer patients with the Swedish amyloid precursor 670/671 mutation. Journal Neurochem.(72).
McGeer, EG. & McGeer, PL.(1997). The role of the immune system in neurodegenerative disorders. Mov Disord.(12).
McGeer, EG. & McGeer, PL.(2003). Inflammatory processes in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry.(27).
Mesulam M. (1995).Structure and function of cholinergic pathways in the cerebral cortex, limbic system, basal ganglia, and thalamus of the human brain. New York: Raven Press.p.139.
Mesulam, M. (2000) Principles of behavioral and cognitive neurology. NewYork: Oxford University Press.
Minton, L. et al.(1997). Somatostatin and neuropeptide Y in cerebrospinal fluid correlations with severity of disease and clinical signs in Alzheimer’s disease and frontotemporal dementia. Dement Geriatr Cogn Disord.(8).
Morillo, L. (2006) Alzheimer: ¿Qué es la Enfermedad?. Abc Medicus. (40).p.4.
Nesse, R. & Williams, G. (1994) Why we get sick. New York: Vintage BooksRandom House.
Nordberg, A. (2001). Nicotonic receptor abnormalities of Alzheimer’s disease:Therapeutic implications. Biol Psychiatry. (49).p.200.
Nordberg, A. et al. (1998). Longterm tacrine treatment in three mild Alzheimer patients: Effects on nicotinic receptors, cerebral blood flow, glucose metabolism, EEG and cognitive abilities. Alzheimer Diseas Assoc Disord. (12).
Paterson,D. & Nordberg, A. (2000). Neural nicotinic receptors in the human brain. Progress in Neurobiology. (61).
Poirier, J.(1994).Apolipoprotein E in animal models of CNS injury and in Alzheimer’s disease. Trends Neurosci.(17).p.528.
Price, JL. et al.(2001). Neuron number in the entorhinal cortex and CAI in preclinical Alzheimer’s disease. Arch Neurol. (58).p.156.
Rogaev, EI. et al.(1995).Familial Alzheimer’s disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer’s disease type 3 gene. Nature. (376).
Schellenberg, GD.et al.(1992).Genetic linkage evidence for a familial Alzheimer’s disease locus on chromosome 14. Science.(258).
Smith, E. et al. (1999) Evolutionary medicine. New York:Oxford University Press. p.25
Strittmatter, WJ.et al.(1993).Apolipoprotein E: high-avidity binding to betaamyloid and increased frequency of type 4 allele in late-onset failial Alzheimer disease. Proc Natl Acad Sci.(90).p.197.
Tárraga, L. et al. “Estimulación cognitiva y memoria” Disponible en red: www.infodoctor.org/alzheimer.htm, extraido el 20 de Abril de 2006}. Toledo, M. (2006) Inflamación y Enfermedad de Alzheimer. Revista de Neurología (42).pp.433, 435.
Thomas, M.& Isaac, M. (1987) Alois Alzheimer: a memoir. Trends Neurosci (10).
Van Broeckhoven, C.et al.(1992). Mapping of a gene predisposing to earlyonset Alzheimer’s disease to chromosome 14q24.3. Nat Genet.(2)
Van Hoesen, GW. & Hyman, BT. (1990) Hippocampal formation: anatomy and the patterns of patholog Alzheimer’s disease. Brain Res (83).p.448.
Vilalta, J. et al. (2000) Prevalencia de demencias en una zona rural. Revista Neurológica. (30).
Wilson, RS. et al.(2002). The apolipoprotein E 4 allele and decline in different cognitive systems during a 6-year period. Arch Neurol.(59).
Zorumski,CF. & Isenberg, KE. (1991) Insights into the structure and function of GABA benzodiazepine receptors: ion channels and psychiatry. American Journal of Psychiatry. (148).p.162.
“Neurología, Enfermedad de Alzheimer” Disponible en red {www.iqb.es/neurologia/enfermedades/alzheimer/enfermedadpaciente/ e003.htm, extraido el 5 de Abril de 2006}
“Historia de una efermedad” Disponible en red {www. elmundosalud.elmundo.es/elmundosalud/especiales/2004/04/alzheimer/ historia.htm, extraido 10 de Marzo de 2006}
“La enfermedad de Alzheimer, Historia” Disponible en red {www.grunenthal.es/cw/es_ES/html/cw_es_es_patient.jhtml?CatId=cw _es_es_patient_d_01b, extraído el 7 de Abril de 2006}
“Stages of Alzheimer's Disease, Alzheimer's Association” Disponible en red {http://www.alz.org/aboutad/stages.asp, extraido 7 de Abril de 2006}
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/10818/2168
dc.identifier.local.none.fl_str_mv 88334
TE04585
identifier_str_mv Algado, M.T., et al.(1997). Familia y enfermedad de Alzheimer.Una perspectiva cualitativa. Anales de Psicología, (13), p.21.
Bartus, RT.(2000) On neurodegenerative diseases, models, and treatment strategies:lessons learned and lessons forgotten a generation following the cholinergic hupothesis. Exp Neurol (163).
Bermejo, FP. (1998) La enfermedad de Alzheimer. Medicina Interna (16).
Blasco, I. & Grubeck-Loebenstein, B.(2003). Role of the immune system in the pathogenesis, prevention and treatment of Alzheimer’s disease. Drugs Aging.(20).p.105.
Blasco, I. et al.(2004). How chronic inflammation affects the brain and supports the development of Alzheimer’s disease in old age: the role of microglia and astrocytes. Aging Cell.(3).
Buffil, E. & Blesa, R. (2006) Alzheimer’s Disease And Brain Evolution: Is Alzheimer's Disease An Example Of Antagonistic Pleiotropy?. Revista de Neurología (42).pp.25-26
Campion, D. et al.(1999). Early-onset autosomal dominant Alzheimer disease: prevalence,genetic heterogeneity, and mutation spectrum. American Journal Hum Genet.(65).p.668.
Cruts, M. & Van Broeckhoven, C.(1998).Presenilin mutations in Alzheimer’s disease.Hum Mutat. (11).
Farrer, LA. et al.(1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis.
APOE and Alzheimer Disease Meta Analysis Consortium. JAMA.(278).p.1350.
Flynn, DD. Et al.(1995). Differential alterations in muscarinic receptor subtypes in Alzheimer’s disease: implications for cholinergicbased therapies. Life Sci (56).p.86.
Forstl, H. et al. (1992).Clinical and neuropathological correlatesof depression in Alzheimer’s disease. Psychol Med.(22).
Gálvez, R. et al. (2000) Epidemiología de la enfermedades degenerativas del sistema nervioso. Barcelona: ed. Masson Salvat-Medicina.
Gómez,T. et al.(1997).Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer’s disease. Ann Neurol. (41).p.19
Gottfries, CG. et al.(1995) Neuropeptides and Alzheimer’s disease. Eur Neuropsychopharmacol.(5).
Hardy, J.et al.(1998).Genetic dissection of Alzheimer’s disease and related dementias: amyloid and its relationship to tau. Nat Neurosci. (1).p.371. Hoenicka, J. (2006) Genes In Alzheimer’s Disease.Rev Neurol.(42).pp.302-303
Huse, JT. & Doms, RW. (2000). Closing in on the amyloid cascade: recent insights into the cell biology of Alzheimer’s disease. Mol Neurobiol. (22).p.88.
Ikonomovic, MD.et al.(1999). Distribution of glutamate receptor subunit NMDAR1 in the hippocampus of normal elderly and patients with Alzheimer’s disease. Exp Neurol.(160)
Kordower, JH. Et al. (2001). Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment. Ann Neurol (49).
Lanctot, KL. et al (2001) Role of serotonin in the behavioraland psychological symptoms of dementia. Journal of Neuropsychiat Clinical. (13).p.521.
Lewis, J. et al.(2001) Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science. (293).
Li, YM. et al.(2000).Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1. Nature.(405)
López, L. & DeKosky, S. (2003). Neuropatología de la enfermedad de Alzheimer y del deterioro cognitivo leve. Revista Neurologica. (37).p158-159.
Maelicke, A. et al.(2000) Allosterically potentiating ligands of nicotinic receptors as a treatment strategy for Alzheimer’s disease. Behav Brain Res. (113).
Martín, CM.et al.(1999). Alpha4 but not Alpha3 and Alpha7 nicotinic acetylcholine receptor subunits are lost from the temporal cortex in Alzheimer’s disease. Journal Neurochem. (73).
Martin, JB.(1999). Molecular basis of the neurodegenerative disorders. New England Journal Med.(340).
Marutle, A, et al.(1999) Neuronal nicotinic receptor deficits in Alzheimer patients with the Swedish amyloid precursor 670/671 mutation. Journal Neurochem.(72).
McGeer, EG. & McGeer, PL.(1997). The role of the immune system in neurodegenerative disorders. Mov Disord.(12).
McGeer, EG. & McGeer, PL.(2003). Inflammatory processes in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry.(27).
Mesulam M. (1995).Structure and function of cholinergic pathways in the cerebral cortex, limbic system, basal ganglia, and thalamus of the human brain. New York: Raven Press.p.139.
Mesulam, M. (2000) Principles of behavioral and cognitive neurology. NewYork: Oxford University Press.
Minton, L. et al.(1997). Somatostatin and neuropeptide Y in cerebrospinal fluid correlations with severity of disease and clinical signs in Alzheimer’s disease and frontotemporal dementia. Dement Geriatr Cogn Disord.(8).
Morillo, L. (2006) Alzheimer: ¿Qué es la Enfermedad?. Abc Medicus. (40).p.4.
Nesse, R. & Williams, G. (1994) Why we get sick. New York: Vintage BooksRandom House.
Nordberg, A. (2001). Nicotonic receptor abnormalities of Alzheimer’s disease:Therapeutic implications. Biol Psychiatry. (49).p.200.
Nordberg, A. et al. (1998). Longterm tacrine treatment in three mild Alzheimer patients: Effects on nicotinic receptors, cerebral blood flow, glucose metabolism, EEG and cognitive abilities. Alzheimer Diseas Assoc Disord. (12).
Paterson,D. & Nordberg, A. (2000). Neural nicotinic receptors in the human brain. Progress in Neurobiology. (61).
Poirier, J.(1994).Apolipoprotein E in animal models of CNS injury and in Alzheimer’s disease. Trends Neurosci.(17).p.528.
Price, JL. et al.(2001). Neuron number in the entorhinal cortex and CAI in preclinical Alzheimer’s disease. Arch Neurol. (58).p.156.
Rogaev, EI. et al.(1995).Familial Alzheimer’s disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer’s disease type 3 gene. Nature. (376).
Schellenberg, GD.et al.(1992).Genetic linkage evidence for a familial Alzheimer’s disease locus on chromosome 14. Science.(258).
Smith, E. et al. (1999) Evolutionary medicine. New York:Oxford University Press. p.25
Strittmatter, WJ.et al.(1993).Apolipoprotein E: high-avidity binding to betaamyloid and increased frequency of type 4 allele in late-onset failial Alzheimer disease. Proc Natl Acad Sci.(90).p.197.
Tárraga, L. et al. “Estimulación cognitiva y memoria” Disponible en red: www.infodoctor.org/alzheimer.htm, extraido el 20 de Abril de 2006}. Toledo, M. (2006) Inflamación y Enfermedad de Alzheimer. Revista de Neurología (42).pp.433, 435.
Thomas, M.& Isaac, M. (1987) Alois Alzheimer: a memoir. Trends Neurosci (10).
Van Broeckhoven, C.et al.(1992). Mapping of a gene predisposing to earlyonset Alzheimer’s disease to chromosome 14q24.3. Nat Genet.(2)
Van Hoesen, GW. & Hyman, BT. (1990) Hippocampal formation: anatomy and the patterns of patholog Alzheimer’s disease. Brain Res (83).p.448.
Vilalta, J. et al. (2000) Prevalencia de demencias en una zona rural. Revista Neurológica. (30).
Wilson, RS. et al.(2002). The apolipoprotein E 4 allele and decline in different cognitive systems during a 6-year period. Arch Neurol.(59).
Zorumski,CF. & Isenberg, KE. (1991) Insights into the structure and function of GABA benzodiazepine receptors: ion channels and psychiatry. American Journal of Psychiatry. (148).p.162.
“Neurología, Enfermedad de Alzheimer” Disponible en red {www.iqb.es/neurologia/enfermedades/alzheimer/enfermedadpaciente/ e003.htm, extraido el 5 de Abril de 2006}
“Historia de una efermedad” Disponible en red {www. elmundosalud.elmundo.es/elmundosalud/especiales/2004/04/alzheimer/ historia.htm, extraido 10 de Marzo de 2006}
“La enfermedad de Alzheimer, Historia” Disponible en red {www.grunenthal.es/cw/es_ES/html/cw_es_es_patient.jhtml?CatId=cw _es_es_patient_d_01b, extraído el 7 de Abril de 2006}
“Stages of Alzheimer's Disease, Alzheimer's Association” Disponible en red {http://www.alz.org/aboutad/stages.asp, extraido 7 de Abril de 2006}
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spelling Suárez Baquero, AlejandraRugeles Castañeda, AndreaPsicólogo2012-05-15T19:16:46Z2012-05-15T19:16:46Z20072012-05-15Algado, M.T., et al.(1997). Familia y enfermedad de Alzheimer.Una perspectiva cualitativa. Anales de Psicología, (13), p.21.Bartus, RT.(2000) On neurodegenerative diseases, models, and treatment strategies:lessons learned and lessons forgotten a generation following the cholinergic hupothesis. Exp Neurol (163).Bermejo, FP. (1998) La enfermedad de Alzheimer. Medicina Interna (16).Blasco, I. & Grubeck-Loebenstein, B.(2003). Role of the immune system in the pathogenesis, prevention and treatment of Alzheimer’s disease. Drugs Aging.(20).p.105.Blasco, I. et al.(2004). How chronic inflammation affects the brain and supports the development of Alzheimer’s disease in old age: the role of microglia and astrocytes. Aging Cell.(3).Buffil, E. & Blesa, R. (2006) Alzheimer’s Disease And Brain Evolution: Is Alzheimer's Disease An Example Of Antagonistic Pleiotropy?. Revista de Neurología (42).pp.25-26Campion, D. et al.(1999). Early-onset autosomal dominant Alzheimer disease: prevalence,genetic heterogeneity, and mutation spectrum. American Journal Hum Genet.(65).p.668.Cruts, M. & Van Broeckhoven, C.(1998).Presenilin mutations in Alzheimer’s disease.Hum Mutat. (11).Farrer, LA. et al.(1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis.APOE and Alzheimer Disease Meta Analysis Consortium. JAMA.(278).p.1350.Flynn, DD. Et al.(1995). Differential alterations in muscarinic receptor subtypes in Alzheimer’s disease: implications for cholinergicbased therapies. Life Sci (56).p.86.Forstl, H. et al. (1992).Clinical and neuropathological correlatesof depression in Alzheimer’s disease. Psychol Med.(22).Gálvez, R. et al. (2000) Epidemiología de la enfermedades degenerativas del sistema nervioso. Barcelona: ed. Masson Salvat-Medicina.Gómez,T. et al.(1997).Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer’s disease. Ann Neurol. (41).p.19Gottfries, CG. et al.(1995) Neuropeptides and Alzheimer’s disease. Eur Neuropsychopharmacol.(5).Hardy, J.et al.(1998).Genetic dissection of Alzheimer’s disease and related dementias: amyloid and its relationship to tau. Nat Neurosci. (1).p.371. Hoenicka, J. (2006) Genes In Alzheimer’s Disease.Rev Neurol.(42).pp.302-303Huse, JT. & Doms, RW. (2000). Closing in on the amyloid cascade: recent insights into the cell biology of Alzheimer’s disease. Mol Neurobiol. (22).p.88.Ikonomovic, MD.et al.(1999). Distribution of glutamate receptor subunit NMDAR1 in the hippocampus of normal elderly and patients with Alzheimer’s disease. Exp Neurol.(160)Kordower, JH. Et al. (2001). Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment. Ann Neurol (49).Lanctot, KL. et al (2001) Role of serotonin in the behavioraland psychological symptoms of dementia. Journal of Neuropsychiat Clinical. (13).p.521.Lewis, J. et al.(2001) Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science. (293).Li, YM. et al.(2000).Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1. Nature.(405)López, L. & DeKosky, S. (2003). Neuropatología de la enfermedad de Alzheimer y del deterioro cognitivo leve. Revista Neurologica. (37).p158-159.Maelicke, A. et al.(2000) Allosterically potentiating ligands of nicotinic receptors as a treatment strategy for Alzheimer’s disease. Behav Brain Res. (113).Martín, CM.et al.(1999). Alpha4 but not Alpha3 and Alpha7 nicotinic acetylcholine receptor subunits are lost from the temporal cortex in Alzheimer’s disease. Journal Neurochem. (73).Martin, JB.(1999). Molecular basis of the neurodegenerative disorders. New England Journal Med.(340).Marutle, A, et al.(1999) Neuronal nicotinic receptor deficits in Alzheimer patients with the Swedish amyloid precursor 670/671 mutation. Journal Neurochem.(72).McGeer, EG. & McGeer, PL.(1997). The role of the immune system in neurodegenerative disorders. Mov Disord.(12).McGeer, EG. & McGeer, PL.(2003). Inflammatory processes in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry.(27).Mesulam M. (1995).Structure and function of cholinergic pathways in the cerebral cortex, limbic system, basal ganglia, and thalamus of the human brain. New York: Raven Press.p.139.Mesulam, M. (2000) Principles of behavioral and cognitive neurology. NewYork: Oxford University Press.Minton, L. et al.(1997). Somatostatin and neuropeptide Y in cerebrospinal fluid correlations with severity of disease and clinical signs in Alzheimer’s disease and frontotemporal dementia. Dement Geriatr Cogn Disord.(8).Morillo, L. (2006) Alzheimer: ¿Qué es la Enfermedad?. Abc Medicus. (40).p.4.Nesse, R. & Williams, G. (1994) Why we get sick. New York: Vintage BooksRandom House.Nordberg, A. (2001). Nicotonic receptor abnormalities of Alzheimer’s disease:Therapeutic implications. Biol Psychiatry. (49).p.200.Nordberg, A. et al. (1998). Longterm tacrine treatment in three mild Alzheimer patients: Effects on nicotinic receptors, cerebral blood flow, glucose metabolism, EEG and cognitive abilities. Alzheimer Diseas Assoc Disord. (12).Paterson,D. & Nordberg, A. (2000). Neural nicotinic receptors in the human brain. Progress in Neurobiology. (61).Poirier, J.(1994).Apolipoprotein E in animal models of CNS injury and in Alzheimer’s disease. Trends Neurosci.(17).p.528.Price, JL. et al.(2001). Neuron number in the entorhinal cortex and CAI in preclinical Alzheimer’s disease. Arch Neurol. (58).p.156.Rogaev, EI. et al.(1995).Familial Alzheimer’s disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer’s disease type 3 gene. Nature. 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(148).p.162.“Neurología, Enfermedad de Alzheimer” Disponible en red {www.iqb.es/neurologia/enfermedades/alzheimer/enfermedadpaciente/ e003.htm, extraido el 5 de Abril de 2006}“Historia de una efermedad” Disponible en red {www. elmundosalud.elmundo.es/elmundosalud/especiales/2004/04/alzheimer/ historia.htm, extraido 10 de Marzo de 2006}“La enfermedad de Alzheimer, Historia” Disponible en red {www.grunenthal.es/cw/es_ES/html/cw_es_es_patient.jhtml?CatId=cw _es_es_patient_d_01b, extraído el 7 de Abril de 2006}“Stages of Alzheimer's Disease, Alzheimer's Association” Disponible en red {http://www.alz.org/aboutad/stages.asp, extraido 7 de Abril de 2006}http://hdl.handle.net/10818/216888334TE0458544 Páginas.El Alzheimer es una enfermedad degenerativa progresiva del cerebro, se manifiesta por la desorientación y perdida de memoria. Fue descrita en 1906, por Alois Alzheimer. Anatomopatológicamente, se caracteriza por la aparición de placas seniles conformadas por la acumulación de la molécula amieloide, producto de la APP. Están implicados los cromosomas 1, 14, 19 y 21. El cromosoma 19, sintetiza la proteína activadora APOE, responsable del inicio de la enfermedad. Se han evidenciado anomalías inmunológicas debido a que la molécula amieloide no suele encontrarse en los vertebrados, por lo tanto éstos carecen de enzimas necesarias para degradarla; ello podría explicar la progresiva acumulación de amieloide; motivo por el cual las células de la microglía se activan pero no responden inmunológicamente.Universidad de La SabanaPsicologíaFacultad de PsicologíaUniversidad de la SabanaIntellectum Repositorio Universidad de la SabanaEnfermedad de AlzheimerEnfermedades del sistema nerviosoAlzheimer: Una mirada neurofisiológica y patológica de la enfermedad. ¿Dónde se origina la enfermedad?bachelorThesisTesis de pregradopublishedVersionhttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_7a1fspahttp://purl.org/coar/access_right/c_abf2ORIGINAL131418.pdf131418.pdfVer documento en PDFapplication/pdf212989https://intellectum.unisabana.edu.co/bitstream/10818/2168/1/131418.pdf87b355c486f1f2ed02293e8a9c4f1fceMD51LICENSElicense.txtlicense.txttext/plain; charset=utf-8498https://intellectum.unisabana.edu.co/bitstream/10818/2168/2/license.txtf52a2cfd4df262e08e9b300d62c85cabMD52TEXT131418.pdf.txt131418.pdf.txtExtracted texttext/plain66438https://intellectum.unisabana.edu.co/bitstream/10818/2168/3/131418.pdf.txt38cf0414036bbd6e592adba053e5161bMD5310818/2168oai:intellectum.unisabana.edu.co:10818/21682019-05-31 10:11:44.654Intellectum Universidad de la Sabanacontactointellectum@unisabana.edu.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