Publication:
The Role of Circulating Aβ Seeds in the Progression of Cerebral Amyloidosis.

dc.contributor.authorGamez, Nazaret
dc.contributor.authorMorales, Rodrigo
dc.date.accessioned2023-05-03T13:32:45Z
dc.date.available2023-05-03T13:32:45Z
dc.date.issued2022-09-15
dc.description.abstractWhile understudied, it is suspected that peripheral Aβ peptides affect Alzheimer's disease (AD)-associated pathological changes in the brain. The peripheral sink hypothesis postulates that the central and peripheral pools of Aβ co-exist in equilibrium. As such, cerebral amyloid levels may be modulated by intervening circulating Aβ. In this commentary, we discuss relevant literature supporting the potential role of peripheral Aβ in exacerbating brain amyloidosis in both humans and mouse models of AD. Moreover, we highlight the need to further understand the mechanisms by which circulating Aβ peptides may reach the brain and contribute to neuropathology. Finally, we discuss the implications of targeting peripheral Aβ as a therapeutic approach in treating AD.
dc.identifier.doi10.1177/26331055221123072
dc.identifier.essn2633-1055
dc.identifier.pmcPMC9493672
dc.identifier.pmid36158163
dc.identifier.pubmedURLhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493672/pdf
dc.identifier.unpaywallURLhttps://doi.org/10.1177/26331055221123072
dc.identifier.urihttp://hdl.handle.net/10668/20243
dc.journal.titleNeuroscience insights
dc.journal.titleabbreviationNeurosci Insights
dc.language.isoen
dc.organizationInstituto de Investigación Biomédica de Málaga-IBIMA
dc.page.number2,63310552211231E+016
dc.pubmedtypeJournal Article
dc.pubmedtypeComment
dc.rightsAttribution-NonCommercial 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subjectAlzheimer’s disease
dc.subjectamyloid-beta
dc.subjectneurodegeneration
dc.subjectperipheral tissues
dc.subjectprion
dc.titleThe Role of Circulating Aβ Seeds in the Progression of Cerebral Amyloidosis.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number17
dspace.entity.typePublication

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