Differentially Aquaporin 5 Expression in Submandibular Glands and Cerebral Cortex in Alzheimer’s Disease

Impaired brain clearance mechanisms may result in the accumulation of aberrant proteins that define Alzheimer’s disease (AD). The water channel protein astrocytic aquaporin 4 (AQP4) is essential for brain amyloid-β clearance, but it is known to be abnormally expressed in AD brains. The expression of...

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Published in:Biomedicines 2022-07, Vol.10 (7), p.1645
Main Authors: Antequera, Desiree, Carrero, Laura, Cunha Alves, Victoria, Ferrer, Isidro, Hernández-Gallego, Jesús, Municio, Cristina, Carro, Eva
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amyloid precursor protein
Animals
Antibodies
Aquaporin 4
Aquaporin 5
Aquaporins
Astrocytes
Brain injury
Brain research
Cell migration
Cerebral cortex
Cytoskeleton
Exocrine glands
Ischemia
Laboratories
Membranes
Nervous system
Neurodegenerative diseases
neurons
Neuropathology
Pathology
Presenilin 1
Proteins
Salivary gland
Software
submandibular gland
β-Amyloid
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Summary:Impaired brain clearance mechanisms may result in the accumulation of aberrant proteins that define Alzheimer’s disease (AD). The water channel protein astrocytic aquaporin 4 (AQP4) is essential for brain amyloid-β clearance, but it is known to be abnormally expressed in AD brains. The expression of AQPs is differentially regulated during diverse brain injuries, but, whereas AQP4 expression and function have been studied in AD, less is known about AQP5. AQP5 functions include not only water transport but also cell migration mediated by cytoskeleton regulation. Moreover, AQP5 has been reported to be expressed in astrocytes, which are regulated after ischemic and traumatic injury. Additionally, AQP5 is particularly abundant in the salivary glands suggesting that it may be a crucial factor in gland dysfunction associated with AD. Herein, we aim to determine whether AQP5 expression in submandibular glands and the brain was altered in AD. First, we demonstrated impaired AQP5 expression in submandibular glands in APP/PS1 mice and AD patients. Subsequently, we observed that AQP5 expression was upregulated in APP/PS1 cerebral cortex and confirmed its expression both in astrocytes and neurons. Our findings propose AQP5 as a significant role player in AD pathology, in addition to AQP4, representing a potential target for the treatment of AD.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines10071645