Abstract
The accumulation of amyloid β (Aβ) in the brain is a major pathological feature of Alzheimer’s disease (AD). In our previous study, we demonstrated that coffee polyphenols (CPP) prevent cognitive dysfunction and Aβ deposition in the brain of an APP/PS2 transgenic mouse AD model. The underlying mechanisms, however, remain to be elucidated. Here, we investigated the effects of the chronic administration of 5-caffeoylquinic acid (5-CQA), the most abundant component of CPP, on cognitive dysfunction in APP/PS2 mice to identify the role of CPP in Aβ elimination. Relative to the untreated controls, the mice fed a 5-CQA-supplemented diet showed significant improvements in their cognitive function assessed by Y-maze and novel object recognition tests. Histochemical analysis revealed that 5-CQA substantially reduced Aβ plaque formation and neuronal loss in the hippocampi. Moreover, 5-CQA upregulated the gene encoding low-density lipoprotein receptor-related protein 1, an Aβ efflux receptor, and normalized the perivascular localization of aquaporin 4, which facilitates Aβ clearance along the paravascular pathway. These results suggest that 5-CQA reduces Aβ deposition in the brain by modulating the Aβ clearance pathways and ameliorating cognitive decline and neuronal loss in APP/PS2 mice. Thus, 5-CQA may be effective in preventing cognitive dysfunction in AD.
Highlights
In 2018, the number of people living with dementia reached approximately 50 million, which is expected to increase to 152 million by 2050 [1]
5-caffeoylquinic acid (5-CQA) upregulated the gene encoding low-density lipoprotein receptor-related protein 1, an amyloid β (Aβ) efflux receptor, and normalized the perivascular localization of aquaporin 4, which facilitates Aβ clearance along the paravascular pathway. These results suggest that 5-CQA reduces Aβ deposition in the brain by modulating the Aβ clearance pathways and ameliorating cognitive decline and neuronal loss in amyloid precursor protein (APP)/PS2 mice
We demonstrated that coffee polyphenols (CPP) comprising caffeoylquinic acids, feruloylquinic acids, and diCQAs prevented cognitive dysfunction and Aβ deposition in the hippocampi of APP/PS2 mice [30]
Summary
In 2018, the number of people living with dementia reached approximately 50 million, which is expected to increase to 152 million by 2050 [1]. The global estimated cost of dementia in 2018 was US$. The most common cause of dementia is Alzheimer’s disease (AD), which is characterized by memory and cognitive dysfunction. The prevalence of AD is increasing globally as the elderly population expands [2,3]. Deposition of amyloid β (Aβ) peptides and aggregation of neurofibrillary tangles in the brain are the major pathological features of AD. They play important roles in AD progression by causing synaptic dysfunction and neuronal cell death [4,5]. Aβ is generated by β- and γ-secretases that mediate the Nutrients 2020, 12, 494; doi:10.3390/nu12020494 www.mdpi.com/journal/nutrients
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