Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/16845
Título
Altered Clock Gene Expression in Female APP/PS1 Mice and Aquaporin-Dependent Amyloid Accumulation in the Retina
Autor(es)
Carrero, Laura | Antequera, Desireé ISCIII | Alcalde, Ignacio | Megías, Diego ISCIII | Ordoñez-Gutierrez, Lara | Gutierrez, Cristina | Merayo-Lloves, Jesús | Wandosell, Francisco | Municio, Cristina | Carro, Eva ISCIII
Fecha de publicación
2023-10-27
Cita
Int J Mol Sci. 2023 Oct 27;24(21):15679.
Idioma
Inglés
Tipo de documento
research article
Resumen
Alzheimer's disease (AD), the most prevalent form of dementia, is a neurodegenerative disorder characterized by different pathological symptomatology, including disrupted circadian rhythm. The regulation of circadian rhythm depends on the light information that is projected from the retina to the suprachiasmatic nucleus in the hypothalamus. Studies of AD patients and AD transgenic mice have revealed AD retinal pathology, including amyloid-β (Aβ) accumulation that can directly interfere with the regulation of the circadian cycle. Although the cause of AD pathology is poorly understood, one of the main risk factors for AD is female gender. Here, we found that female APP/PS1 mice at 6- and 12-months old display severe circadian rhythm disturbances and retinal pathological hallmarks, including Aβ deposits in retinal layers. Since brain Aβ transport is facilitated by aquaporin (AQP)4, the expression of AQPs were also explored in APP/PS1 retina to investigate a potential correlation between retinal Aβ deposits and AQPs expression. Important reductions in AQP1, AQP4, and AQP5 were detected in the retinal tissue of these transgenic mice, mainly at 6-months of age. Taken together, our findings suggest that abnormal transport of Aβ, mediated by impaired AQPs expression, contributes to the retinal degeneration in the early stages of AD.
Palabras clave
Alzheimer’s disease | Circadian rhythm | Clock genes | Retina | Transgenic mice | Hypothalamus | Cerebral cortex | Hippocampus | Amyloid
MESH
Amyloid beta-Protein Precursor | Alzheimer Disease | Mice | Humans | Female | Animals | Infant | Amyloid beta-Peptides | Mice, Transgenic | Retina | Aquaporin 4 | Gene Expression | Disease Models, Animal | Presenilin-1 | Plaque, Amyloid
Versión en línea
DOI
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