Can We Treat Neuroinflammation in Alzheimer's Disease?
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Altres documents de l'autoria: Sánchez-Sarasúa, Sandra; Fernández-Pérez, Iván; Espinosa-Fernández, Verónica; Sánchez-Pérez, Ana María; Ledesma, Juan Carlos
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Mostra el registre complet de l'elementcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/36080
comunitat-uji-handle3:10234/36082
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INVESTIGACIONMetadades
Títol
Can We Treat Neuroinflammation in Alzheimer's Disease?Autoria
Data de publicació
2020-11-19Editor
MDPIISSN
1422-0067Cita bibliogràfica
Sánchez-Sarasúa, Sandra; Fernández-Pérez, Iván; Espinosa-Fernández, Verónica; Sánchez-Pérez, Ana M.; Ledesma, Juan C. 2020. "Can We Treat Neuroinflammation in Alzheimer’s Disease?" Int. J. Mol. Sci. 21, no. 22: 8751.Tipus de document
info:eu-repo/semantics/articleVersió de l'editorial
https://www.mdpi.com/1422-0067/21/22/8751Versió
info:eu-repo/semantics/publishedVersionParaules clau / Matèries
Resum
Alzheimer’s disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid ... [+]
Alzheimer’s disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid depression and aggressiveness. Aging is the major factor contributing to AD; however, the initial cause that triggers the disease is yet unknown. Scientific evidence demonstrates that AD, especially the late onset of AD, is not the result of a single event, but rather it appears because of a combination of risk elements with the lack of protective ones. A major risk factor underlying the disease is neuroinflammation, which can be activated by different situations, including chronic pathogenic infections, prolonged stress and metabolic syndrome. Consequently, many therapeutic strategies against AD have been designed to reduce neuro-inflammation, with very promising results improving cognitive function in preclinical models of the disease. The literature is massive; thus, in this review we will revise the translational evidence of these early strategies focusing in anti-diabetic and anti-inflammatory molecules and discuss their therapeutic application in humans. Furthermore, we review the preclinical and clinical data of nutraceutical application against AD symptoms. Finally, we introduce new players underlying neuroinflammation in AD: the activity of the endocannabinoid system and the intestinal microbiota as neuroprotectors. This review highlights the importance of a broad multimodal approach to treat successfully the neuroinflammation underlying AD. [-]
Publicat a
Int. J. Mol. Sci. 2020, 21, 8751Proyecto de investigación
UJI-B2018-01 to AMSP; ACIF/2016/250 to SSSDrets d'accés
© 2020 by the authors. Licensee MDPI, Basel, Switzerland
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/openAccess
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