Abnormal platelet amyloid-ß precursor protein metabolism in SAMP8 mice: Evidence for peripheral marker in Alzheimer's disease.
J Cell Physiol
; 234(12): 23528-23536, 2019 12.
Article
en En
| MEDLINE
| ID: mdl-31183859
ABSTRACT
Senescence-accelerated mouse strains have proved to be an accelerated-aging model, which mimics numerous features with Alzheimer's disease (AD). Three, six, and nine-month senescence-accelerated resistant 1 and senescence-accelerated prone 8 (SAMP8) mice were used in the current study, to unravel potential mechanisms for dementia and explore new diagnostic approaches for AD. The amyloid-ß (Aß40) and Aß42 levels were elevated in hippocampi and platelets from SAMP8, along with a reduced α-secretase expression and an enhanced ß-secretase expression extent with age, compared to control mice. Furthermore, hippocampal Aß40 and Aß42 of SAMP8 were positively correlated with platelet of these mice with aging progression. In addition, ß-γ-secretase-modulated proteolytic proceeding of amyloid precursor protein in platelet might work through the PI3K/Akt/GSK3ß pathway. These results indicate that platelet could be a potential early marker in the periphery to study the age-correlative aggregation of the amyloid-ß peptide in patients with AD, while still requiring the considerable study.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Fragmentos de Péptidos
/
Plaquetas
/
Péptidos beta-Amiloides
/
Enfermedad de Alzheimer
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Cell Physiol
Año:
2019
Tipo del documento:
Article
País de afiliación:
China