Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions

Objective: We aim to explain why salivary lactoferrin (Lf) levels are reduced in patients suffering mild cognitive impairment (MCI) and sporadic Alzheimer’s disease (sAD).1 We also will discuss if such Lf decrease could be due to a downregulation of the sAD associated systemic immunity. Background:...

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Detalles Bibliográficos
Autores: Bermejo-Pareja, Félix, Ser, Teodoro del, Valentí, Meritxell, Fuente del Rey, Mónica de la, Bartolomé, Fernando, Carro, Eva
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/6594
Acceso en línea:https://hdl.handle.net/20.500.14352/6594
Access Level:acceso abierto
Palabra clave:612.8
616.894-053.9
Alzheimer’s disease
Amyloid
Biomarkers
Brain-immunity interactions
Hypothalamus
Immunity
Lactoferrin
Saliva
Neurociencias (Biológicas)
2490 Neurociencias
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oai_identifier_str oai:docta.ucm.es:20.500.14352/6594
network_acronym_str ES
network_name_str España
repository_id_str
spelling Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactionsBermejo-Pareja, FélixSer, Teodoro delValentí, MeritxellFuente del Rey, Mónica de laBartolomé, FernandoCarro, Eva612.8616.894-053.9Alzheimer’s diseaseAmyloidBiomarkersBrain-immunity interactionsHypothalamusImmunityLactoferrinSalivaNeurociencias (Biológicas)2490 NeurocienciasObjective: We aim to explain why salivary lactoferrin (Lf) levels are reduced in patients suffering mild cognitive impairment (MCI) and sporadic Alzheimer’s disease (sAD).1 We also will discuss if such Lf decrease could be due to a downregulation of the sAD associated systemic immunity. Background: Several non-neurological alterations have been described in sAD, mainly in skin, blood cell, and immunological capacities. We reviewed briefly the main pathophysiological theories of sAD (amyloid cascade, tau, unfolder protein tau, and amyloid deposits) emphasizing the most brain based hypotheses such as the updated tau-related neuron skeletal hypothesis; we also comment on the systemic theories that emphasize the fetal origin of the complex disorders that include the low inflammatory and immunity theories of sAD. New/updated hypothesis: Lf has important anti-infectious and immunomodulatory roles in health and disease. We present the hypothesis that the reduced levels of saliva Lf could be an effect of immunological disturbances associated to sAD. Under this scenario, two alternative pathways are possible: first, whether sAD could be a systemic disorder (or disorders) related to early immunological and low inflammatory alterations; second, if systemic immunity alterations of sAD manifestations could be downstream of early sAD brain affectations. Major challenges for the hypothesis: The major challenge of the Lf as early sAD biomarker would be its validation in other clinical and population-based studies. It is possible the decreased salivary Lf in early sAD could be related to immunological modulation actions, but other different unknown mechanisms could be the origin of such reduction. Linkage to other major theories:This hypothesis is in agreement with two physiopathological explanations of the sAD as a downstream process determined by the early lesions of the hypothalamus and autonomic vegetative system (neurodegeneration), or as a consequence of low neuroinflammation and dysimmunity since the early life aggravated in the elderly (immunosenescence)WileyUniversidad Complutense de Madrid20202020-06-1620202020-06-16journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/6594reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución-NoComercial 3.0 Españahttps://creativecommons.org/licenses/by-nc/3.0/es/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/65942026-06-02T12:44:21Z
dc.title.none.fl_str_mv Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
title Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
spellingShingle Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
Bermejo-Pareja, Félix
612.8
616.894-053.9
Alzheimer’s disease
Amyloid
Biomarkers
Brain-immunity interactions
Hypothalamus
Immunity
Lactoferrin
Saliva
Neurociencias (Biológicas)
2490 Neurociencias
title_short Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
title_full Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
title_fullStr Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
title_full_unstemmed Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
title_sort Salivary lactoferrin as biomarker for Alzheimer’s disease: brain-immunity interactions
dc.creator.none.fl_str_mv Bermejo-Pareja, Félix
Ser, Teodoro del
Valentí, Meritxell
Fuente del Rey, Mónica de la
Bartolomé, Fernando
Carro, Eva
author Bermejo-Pareja, Félix
author_facet Bermejo-Pareja, Félix
Ser, Teodoro del
Valentí, Meritxell
Fuente del Rey, Mónica de la
Bartolomé, Fernando
Carro, Eva
author_role author
author2 Ser, Teodoro del
Valentí, Meritxell
Fuente del Rey, Mónica de la
Bartolomé, Fernando
Carro, Eva
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 612.8
616.894-053.9
Alzheimer’s disease
Amyloid
Biomarkers
Brain-immunity interactions
Hypothalamus
Immunity
Lactoferrin
Saliva
Neurociencias (Biológicas)
2490 Neurociencias
topic 612.8
616.894-053.9
Alzheimer’s disease
Amyloid
Biomarkers
Brain-immunity interactions
Hypothalamus
Immunity
Lactoferrin
Saliva
Neurociencias (Biológicas)
2490 Neurociencias
description Objective: We aim to explain why salivary lactoferrin (Lf) levels are reduced in patients suffering mild cognitive impairment (MCI) and sporadic Alzheimer’s disease (sAD).1 We also will discuss if such Lf decrease could be due to a downregulation of the sAD associated systemic immunity. Background: Several non-neurological alterations have been described in sAD, mainly in skin, blood cell, and immunological capacities. We reviewed briefly the main pathophysiological theories of sAD (amyloid cascade, tau, unfolder protein tau, and amyloid deposits) emphasizing the most brain based hypotheses such as the updated tau-related neuron skeletal hypothesis; we also comment on the systemic theories that emphasize the fetal origin of the complex disorders that include the low inflammatory and immunity theories of sAD. New/updated hypothesis: Lf has important anti-infectious and immunomodulatory roles in health and disease. We present the hypothesis that the reduced levels of saliva Lf could be an effect of immunological disturbances associated to sAD. Under this scenario, two alternative pathways are possible: first, whether sAD could be a systemic disorder (or disorders) related to early immunological and low inflammatory alterations; second, if systemic immunity alterations of sAD manifestations could be downstream of early sAD brain affectations. Major challenges for the hypothesis: The major challenge of the Lf as early sAD biomarker would be its validation in other clinical and population-based studies. It is possible the decreased salivary Lf in early sAD could be related to immunological modulation actions, but other different unknown mechanisms could be the origin of such reduction. Linkage to other major theories:This hypothesis is in agreement with two physiopathological explanations of the sAD as a downstream process determined by the early lesions of the hypothalamus and autonomic vegetative system (neurodegeneration), or as a consequence of low neuroinflammation and dysimmunity since the early life aggravated in the elderly (immunosenescence)
publishDate 2020
dc.date.none.fl_str_mv 2020
2020-06-16
2020
2020-06-16
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/6594
url https://hdl.handle.net/20.500.14352/6594
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución-NoComercial 3.0 España
https://creativecommons.org/licenses/by-nc/3.0/es/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución-NoComercial 3.0 España
https://creativecommons.org/licenses/by-nc/3.0/es/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300724

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