Mind and memory: a multidisciplinary exploration of Alzheimer's disease.

Detalhes bibliográficos
Autor(a) principal: Zanuto, Bruno
Data de Publicação: 2023
Outros Autores: Bosch, Ana Luiza, Kawaguti, Beatriz Barreira Nunes Rodrigues, Ramo, Daiana de Freitas Ferreira, Nery, Daniela Luiz, Rocha, Hiago Silva, Pinho, Lênio Airam de, Cortês, Mychelle Christian, Lobo, Nayara Silva, Melo, Victorya Machado Silva de
Tipo de documento: Artigo
Idioma: por
Título da fonte: Brazilian Journal of Implantology and Health Sciences
Texto Completo: https://bjihs.emnuvens.com.br/bjihs/article/view/495
Resumo: AD is a neurodegenerative disease and is one of the leading causes of death globally, accounting for more than 4% of deaths in 2016. The dementia-related death rate from AD was more than 45 per 100,000 in a 2013 European study. The prevalence of atypical AD, most common in individuals under 65 years of age, ranges from 15-65/100,000, with some patients experiencing visual or motor difficulties, executive dysfunction, and other symptoms. The pathogenesis of AD is linked to the presence of clusters of extracellular amyloid beta (Aβ) protein, known as neuritic plaques, and tangles of hyperphosphorylated tau proteins. These plaques are formed from amyloid precursor protein (APP) by the action of enzymes, while neurofibrillary tangles consist mainly of hyperphosphorylated tau protein. The relationship between Aβ and tau is synergistic in neurotoxicity, with evidence that Aβ can trigger the formation of tau tangles. Biometals such as iron, copper and zinc have also been linked to AD, with dysregulation of these metals contributing to nervous system toxicity. Genetic factors, including the APOE gene and mutations in the APP, PSEN-1, and PSEN-2 genes, also play an important role in AD. The presence of the APOE ε4 allele significantly increases the risk of developing the disease. Mutations in the APP gene are associated with an accumulation of Aβ, while mutations in PSEN-1 and PSEN-2 affect Aβ production. Clinical manifestations include memory loss, depression, anxiety, language disorders and other cognitive and behavioral changes. The phase of AD varies from preclinical to severe, progressively affecting the patient's daily functioning. Diagnosis combines clinical assessment, neuropsychological tests and biomarkers such as tau protein, Aβ42 and brain imaging. Treatment involves medications such as acetylcholinesterase inhibitors and memantine, as well as therapies being studied that target Aβ proteins. Healthy lifestyles, such as physical activity and diet, also play an important role in preventing and treating AD.
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spelling Mind and memory: a multidisciplinary exploration of Alzheimer's disease.Mente y memoria: una exploración multidisciplinaria de la enfermedad de Alzheimer.Mente e memória : uma exploração multidisciplinar da doença de Alzheimer.doença de AlzheimerdemenciamemóriaAlzheimer's diseasedementiamemoryenfermedad de alzheimerlocuramemoriaAD is a neurodegenerative disease and is one of the leading causes of death globally, accounting for more than 4% of deaths in 2016. The dementia-related death rate from AD was more than 45 per 100,000 in a 2013 European study. The prevalence of atypical AD, most common in individuals under 65 years of age, ranges from 15-65/100,000, with some patients experiencing visual or motor difficulties, executive dysfunction, and other symptoms. The pathogenesis of AD is linked to the presence of clusters of extracellular amyloid beta (Aβ) protein, known as neuritic plaques, and tangles of hyperphosphorylated tau proteins. These plaques are formed from amyloid precursor protein (APP) by the action of enzymes, while neurofibrillary tangles consist mainly of hyperphosphorylated tau protein. The relationship between Aβ and tau is synergistic in neurotoxicity, with evidence that Aβ can trigger the formation of tau tangles. Biometals such as iron, copper and zinc have also been linked to AD, with dysregulation of these metals contributing to nervous system toxicity. Genetic factors, including the APOE gene and mutations in the APP, PSEN-1, and PSEN-2 genes, also play an important role in AD. The presence of the APOE ε4 allele significantly increases the risk of developing the disease. Mutations in the APP gene are associated with an accumulation of Aβ, while mutations in PSEN-1 and PSEN-2 affect Aβ production. Clinical manifestations include memory loss, depression, anxiety, language disorders and other cognitive and behavioral changes. The phase of AD varies from preclinical to severe, progressively affecting the patient's daily functioning. Diagnosis combines clinical assessment, neuropsychological tests and biomarkers such as tau protein, Aβ42 and brain imaging. Treatment involves medications such as acetylcholinesterase inhibitors and memantine, as well as therapies being studied that target Aβ proteins. Healthy lifestyles, such as physical activity and diet, also play an important role in preventing and treating AD.La EA es una enfermedad neurodegenerativa y es una de las principales causas de muerte a nivel mundial, representando más del 4% de las muertes en 2016. La tasa de mortalidad relacionada con la demencia por EA fue de más de 45 por 100.000 en un estudio europeo de 2013. La prevalencia de la EA atípica, más común en personas menores de 65 años, oscila entre 15 y 65/100.000, y algunos pacientes experimentan dificultades visuales o motoras, disfunción ejecutiva y otros síntomas. La patogénesis de la EA está relacionada con la presencia de grupos de proteína beta amiloide extracelular (Aβ), conocidas como placas neuríticas, y ovillos de proteínas tau hiperfosforiladas. Estas placas se forman a partir de la proteína precursora de amiloide (APP) por la acción de enzimas, mientras que los ovillos neurofibrilares están formados principalmente por proteína tau hiperfosforilada. La relación entre Aβ y tau es sinérgica en la neurotoxicidad, con evidencia de que Aβ puede desencadenar la formación de ovillos de tau. Biometales como el hierro, el cobre y el zinc también se han relacionado con la EA, y la desregulación de estos metales contribuye a la toxicidad del sistema nervioso. Los factores genéticos, incluido el gen APOE y las mutaciones en los genes APP, PSEN-1 y PSEN-2, también desempeñan un papel importante en la EA. La presencia del alelo APOE ε4 aumenta significativamente el riesgo de desarrollar la enfermedad. Las mutaciones en el gen APP se asocian con una acumulación de Aβ, mientras que las mutaciones en PSEN-1 y PSEN-2 afectan la producción de Aβ. Las manifestaciones clínicas incluyen pérdida de memoria, depresión, ansiedad, trastornos del lenguaje y otros cambios cognitivos y conductuales. La fase de la EA varía desde preclínica hasta grave, afectando progresivamente el funcionamiento diario del paciente. El diagnóstico combina la evaluación clínica, pruebas neuropsicológicas y biomarcadores como la proteína tau, el Aβ42 y las imágenes cerebrales. El tratamiento incluye medicamentos como inhibidores de la acetilcolinesterasa y memantina, así como terapias en estudio dirigidas a las proteínas Aβ. Los estilos de vida saludables, como la actividad física y la dieta, también desempeñan un papel importante en la prevención y el tratamiento de la EA.A DA é uma doença neurodegenerativa, sendo uma das principais causas de morte global, respondendo por mais de 4% das mortes em 2016. A taxa de mortalidade relacionada à demência da DA foi de mais de 45 por 100.000 em um estudo europeu de 2013. A prevalência da DA atípica, mais comum em indivíduos com menos de 65 anos, varia entre 15-65/100.000, com alguns pacientes apresentando dificuldades visuais ou motoras, disfunção executiva e outros sintomas. A patogênese da DA está ligada à presença de aglomerados de proteína beta-amiloide (Aβ) extracelular, conhecidos como placas neuríticas, e emaranhados de proteínas tau hiperfosforiladas. Essas placas são formadas a partir da proteína precursora de amiloide (APP) por ação de enzimas, enquanto os emaranhados neurofibrilares consistem principalmente de proteína tau hiperfosforilada. A relação entre Aβ e tau é sinérgica na neurotoxicidade, com evidências de que o Aβ pode desencadear a formação de emaranhados de tau. Biometais como ferro, cobre e zinco também foram associados à DA, com a desregulação desses metais contribuindo para a toxicidade do sistema nervoso. Fatores genéticos, incluindo o gene APOE e mutações nos genes APP, PSEN-1 e PSEN-2, também desempenham um papel importante na DA. A presença do alelo APOE ε4 aumenta significativamente o risco de desenvolver a doença. Mutações no gene APP estão associadas a um acúmulo de Aβ, enquanto mutações em PSEN-1 e PSEN-2 afetam a produção de Aβ. As manifestações clínicas incluem perda de memória, depressão, ansiedade, distúrbios de linguagem e outras alterações cognitivas e comportamentais. A fase da DA varia de pré-clínica a grave, afetando progressivamente o funcionamento diário do paciente. O diagnóstico combina avaliação clínica, testes neuropsicológicos e biomarcadores, como proteína tau, Aβ42 e imagens cerebrais. O tratamento envolve medicamentos como inibidores da acetilcolinesterase e memantina, além de terapias em estudo que visam as proteínas Aβ. Estilos de vida saudáveis, como atividade física e dieta, também desempenham um papel importante na prevenção e tratamento da DA.Specialized Dentistry Group2023-09-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://bjihs.emnuvens.com.br/bjihs/article/view/49510.36557/2674-8169.2023v5n4p1695-1709Brazilian Journal of Implantology and Health Sciences ; Vol. 5 No. 4 (2023): BJIHS QUALIS B3; 1695-1709Brazilian Journal of Implantology and Health Sciences ; Vol. 5 Núm. 4 (2023): BJIHS QUALIS B3; 1695-1709Brazilian Journal of Implantology and Health Sciences ; v. 5 n. 4 (2023): BJIHS QUALIS B3; 1695-17092674-8169reponame:Brazilian Journal of Implantology and Health Sciencesinstname:Grupo de Odontologia Especializada (GOE)instacron:GOEporhttps://bjihs.emnuvens.com.br/bjihs/article/view/495/605Copyright (c) 2023 Bruno Zanuto, Ana Luiza Bosch, Beatriz Barreira Nunes Rodrigues Kawaguti, Daiana de Freitas Ferreira Ramo, Daniela Luiz Nery, Hiago Silva Rocha, Lênio Airam de Pinho, Mychelle Christan Cortês, Nayara Silva Lobo, Victorya Machado Silva de Melohttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessZanuto, BrunoBosch, Ana LuizaKawaguti, Beatriz Barreira Nunes RodriguesRamo, Daiana de Freitas FerreiraNery, Daniela LuizRocha, Hiago SilvaPinho, Lênio Airam deCortês, Mychelle ChristianLobo, Nayara SilvaMelo, Victorya Machado Silva de2023-09-12T08:38:51Zoai:ojs.bjihs.emnuvens.com.br:article/495Revistahttps://bjihs.emnuvens.com.br/bjihsONGhttps://bjihs.emnuvens.com.br/bjihs/oaijournal.bjihs@periodicosbrasil.com.br2674-81692674-8169opendoar:2023-09-12T08:38:51Brazilian Journal of Implantology and Health Sciences - Grupo de Odontologia Especializada (GOE)false
dc.title.none.fl_str_mv Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
Mente y memoria: una exploración multidisciplinaria de la enfermedad de Alzheimer.
Mente e memória : uma exploração multidisciplinar da doença de Alzheimer.
title Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
spellingShingle Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
Zanuto, Bruno
doença de Alzheimer
demencia
memória
Alzheimer's disease
dementia
memory
enfermedad de alzheimer
locura
memoria
title_short Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
title_full Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
title_fullStr Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
title_full_unstemmed Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
title_sort Mind and memory: a multidisciplinary exploration of Alzheimer's disease.
author Zanuto, Bruno
author_facet Zanuto, Bruno
Bosch, Ana Luiza
Kawaguti, Beatriz Barreira Nunes Rodrigues
Ramo, Daiana de Freitas Ferreira
Nery, Daniela Luiz
Rocha, Hiago Silva
Pinho, Lênio Airam de
Cortês, Mychelle Christian
Lobo, Nayara Silva
Melo, Victorya Machado Silva de
author_role author
author2 Bosch, Ana Luiza
Kawaguti, Beatriz Barreira Nunes Rodrigues
Ramo, Daiana de Freitas Ferreira
Nery, Daniela Luiz
Rocha, Hiago Silva
Pinho, Lênio Airam de
Cortês, Mychelle Christian
Lobo, Nayara Silva
Melo, Victorya Machado Silva de
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Zanuto, Bruno
Bosch, Ana Luiza
Kawaguti, Beatriz Barreira Nunes Rodrigues
Ramo, Daiana de Freitas Ferreira
Nery, Daniela Luiz
Rocha, Hiago Silva
Pinho, Lênio Airam de
Cortês, Mychelle Christian
Lobo, Nayara Silva
Melo, Victorya Machado Silva de
dc.subject.por.fl_str_mv doença de Alzheimer
demencia
memória
Alzheimer's disease
dementia
memory
enfermedad de alzheimer
locura
memoria
topic doença de Alzheimer
demencia
memória
Alzheimer's disease
dementia
memory
enfermedad de alzheimer
locura
memoria
description AD is a neurodegenerative disease and is one of the leading causes of death globally, accounting for more than 4% of deaths in 2016. The dementia-related death rate from AD was more than 45 per 100,000 in a 2013 European study. The prevalence of atypical AD, most common in individuals under 65 years of age, ranges from 15-65/100,000, with some patients experiencing visual or motor difficulties, executive dysfunction, and other symptoms. The pathogenesis of AD is linked to the presence of clusters of extracellular amyloid beta (Aβ) protein, known as neuritic plaques, and tangles of hyperphosphorylated tau proteins. These plaques are formed from amyloid precursor protein (APP) by the action of enzymes, while neurofibrillary tangles consist mainly of hyperphosphorylated tau protein. The relationship between Aβ and tau is synergistic in neurotoxicity, with evidence that Aβ can trigger the formation of tau tangles. Biometals such as iron, copper and zinc have also been linked to AD, with dysregulation of these metals contributing to nervous system toxicity. Genetic factors, including the APOE gene and mutations in the APP, PSEN-1, and PSEN-2 genes, also play an important role in AD. The presence of the APOE ε4 allele significantly increases the risk of developing the disease. Mutations in the APP gene are associated with an accumulation of Aβ, while mutations in PSEN-1 and PSEN-2 affect Aβ production. Clinical manifestations include memory loss, depression, anxiety, language disorders and other cognitive and behavioral changes. The phase of AD varies from preclinical to severe, progressively affecting the patient's daily functioning. Diagnosis combines clinical assessment, neuropsychological tests and biomarkers such as tau protein, Aβ42 and brain imaging. Treatment involves medications such as acetylcholinesterase inhibitors and memantine, as well as therapies being studied that target Aβ proteins. Healthy lifestyles, such as physical activity and diet, also play an important role in preventing and treating AD.
publishDate 2023
dc.date.none.fl_str_mv 2023-09-11
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
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dc.identifier.uri.fl_str_mv https://bjihs.emnuvens.com.br/bjihs/article/view/495
10.36557/2674-8169.2023v5n4p1695-1709
url https://bjihs.emnuvens.com.br/bjihs/article/view/495
identifier_str_mv 10.36557/2674-8169.2023v5n4p1695-1709
dc.language.iso.fl_str_mv por
language por
dc.relation.none.fl_str_mv https://bjihs.emnuvens.com.br/bjihs/article/view/495/605
dc.rights.driver.fl_str_mv https://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Specialized Dentistry Group
publisher.none.fl_str_mv Specialized Dentistry Group
dc.source.none.fl_str_mv Brazilian Journal of Implantology and Health Sciences ; Vol. 5 No. 4 (2023): BJIHS QUALIS B3; 1695-1709
Brazilian Journal of Implantology and Health Sciences ; Vol. 5 Núm. 4 (2023): BJIHS QUALIS B3; 1695-1709
Brazilian Journal of Implantology and Health Sciences ; v. 5 n. 4 (2023): BJIHS QUALIS B3; 1695-1709
2674-8169
reponame:Brazilian Journal of Implantology and Health Sciences
instname:Grupo de Odontologia Especializada (GOE)
instacron:GOE
instname_str Grupo de Odontologia Especializada (GOE)
instacron_str GOE
institution GOE
reponame_str Brazilian Journal of Implantology and Health Sciences
collection Brazilian Journal of Implantology and Health Sciences
repository.name.fl_str_mv Brazilian Journal of Implantology and Health Sciences - Grupo de Odontologia Especializada (GOE)
repository.mail.fl_str_mv journal.bjihs@periodicosbrasil.com.br
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