Abstract
Deterioration in cognitive abilities, especially memory, is characteristic of Alzheimer's disease (AD), a type of neurodegenerative disease. AD's pathological lesions include intracellular neurofibrillary tangles and extracellular amyloid-β plaques. So far, many efforts have been made to find a cure for AD, but there are still no effective pharmacotherapeutic options that relieve the symptoms and enhance the life quality of AD patients. The intranasal (IN) route has been previously used to treat a wide variety of central nervous system disorders as it is a direct, non-invasive method for delivering drugs to the brain. Our prior in vivo preclinical research employing a rat model of AD revealed that intranasally administered interferon-beta (IFNβ) exhibited pro-cognitive and protective benefits. Therefore, we hypothesize that IN administration of IFNβ can be an effective and promising strategy to slow down cognitive decline in AD patients at least partly by reducing amyloid deposition and tau hyperphosphorylated protein accumulation, promoting anti-inflammatory response and anti-apoptotic pathways, increasing neurotrophic factor expression, activating mitochondrial biogenesis, modulating neurogenesis, and improving cerebral glucose metabolism.
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