The transmembrane amyloid precursor C99 protein exhibits non-specific interaction with tau

Britton, Rhett J.; Hutchison, J.M.S.; Sanders, Charles R.

doi:10.1016/j.bbrc.2021.08.075

Cited by 2 publications

(1 citation statement)

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“…The connection between amyloid and tau protein pathologies is elusive and many studies have been reported the presence of Aβ in inducing tau protein pathology. Interestingly, a recent study has suggested that C99 exhibits nonspecific interaction with tau protein even though it is inconsistent with some previous reports which need to be further investigated (Britton et al, 2021). A recent finding has indicated that Aβ peptides accumulated in endo-lysosomal vesicles at low pH accelerates the formation of Aβ oligomers and potentially induces tau-missorting which involves in AD-associated pathogenesis (Schützmann et al, 2021).…”

Section: Aβ Production and Clearancementioning

confidence: 87%

Beyond the classical amyloid hypothesis in Alzheimer's disease: Molecular insights into current concepts of pathogenesis, therapeutic targets, and study models

Theerasri

Janpaijit

Tencomnao

et al. 2022

WIREs Mechanisms of Disease

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Alzheimer's disease (AD) is one of the progressive neurodegenerative disorders and the most common cause of dementia in the elderly worldwide causing difficulties in the daily life of the patient. AD is characterized by the aberrant accumulation of β-amyloid plaques and tau protein-containing neurofibrillary tangles (NFTs) in the brain giving rise to neuroinflammation, oxidative stress, synaptic failure, and eventual neuronal cell death. The total cost of care in AD treatment and related health care activities is enormous and pharmaceutical drugs approved by Food and Drug Administration have not manifested sufficient efficacy in protection and therapy. In recent years, there are growing studies that contribute a fundamental understanding to AD pathogenesis, ADassociated risk factors, and pharmacological intervention. However, greater molecular process-oriented research in company with suitable experimental models is still of the essence to enhance the prospects for AD therapy and cell lines as a disease model are still the major part of this milestone. In this review, we provide an insight into molecular mechanisms, particularly the recent concept in gut-brain axis, vascular dysfunction and autophagy, and current models used in the study of AD. Here, we emphasized the importance of therapeutic strategy targeting multiple mechanisms together with utilizing appropriate models for the discovery of novel effective AD therapy.

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Section: Aβ Production and Clearancementioning

confidence: 87%