Web of Science: 85 cites, Scopus: 96 cites, Google Scholar: cites,
Amyloid-beta peptide and tau protein crosstalk in Alzheimer's disease
Ramos Roda, Alejandro (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Serra-Mir, Gabriel (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Montoliu-Gaya, Laia (University of Gothenburg)
Tiessler, Lidia (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Villegas Hernández, Sandra (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)

Data: 2022
Resum: Alzheimer's disease is a neurodegenerative disease that accounts for most of the 50-million dementia cases worldwide in 2018. A large amount of evidence supports the amyloid cascade hypothesis, which states that amyloid-beta accumulation triggers tau hyperphosphorylation and aggregation in form of neurofibrillary tangles, and these aggregates lead to inflammation, synaptic impairment, neuronal loss, and thus to cognitive decline and behavioral abnormalities. The poor correlation found between cognitive decline and amyloid plaques, have led the scientific community to question whether amyloid-beta accumulation is actually triggering neurodegeneration in Alzheimer's disease. The occurrence of tau neurofibrillary tangles better correlates to neuronal loss and clinical symptoms and, although amyloid-beta may initiate the cascade of events, tau impairment is likely the effector molecule of neurodegeneration. Recently, it has been shown that amyloid-beta and tau cooperatively work to impair transcription of genes involved in synaptic function and, more importantly, that downregulation of tau partially reverses transcriptional perturbations. Despite mounting evidence points to an interplay between amyloid-beta and tau, some factors could independently affect both pathologies. Thus, the dual pathway hypothesis, which states that there are common upstream triggers causing both amyloid-beta and tau abnormalities has been proposed. Among others, the immune system seems to be strongly involved in amyloid-beta and tau pathologies. Other factors, as the apolipoprotein E ε4 isoform has been suggested to act as a link between amyloid-beta and tau hyperphosphorylation. Interestingly, amyloid-beta-immunotherapy reduces not only amyloid-beta but also tau levels in animal models and in clinical trials. Likewise, it has been shown that tau-immunotherapy also reduces amyloid-beta levels. Thus, even though amyloid-beta immunotherapy is more advanced than tau-immunotherapy, combined amyloid-beta and tau-directed therapies at early stages of the disease have recently been proposed as a strategy to stop the progression of Alzheimer's disease.
Ajuts: Agencia Estatal de Investigación SAF2017-89613-R
Drets: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra, i la creació d'obres derivades, sempre que no sigui amb finalitats comercials i que es distribueixin sota la mateixa llicència que regula l'obra original. Cal que es reconegui l'autoria de l'obra original. Creative Commons
Llengua: Anglès
Document: Article de revisió ; recerca ; Versió publicada
Matèria: Aggregation ; Alzheimer ; Amyloid-beta ; Dementia ; Immunotherapy ; Inflammation ; Neurodegeneration ; Tau
Publicat a: Neural Regeneration Research, Vol. 17, Num. 8 (August 2022) , p. 1666-1674, ISSN 1876-7958

DOI: 10.4103/1673-5374.332127
PMID: 35017413

9 p, 3.7 MB

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