Abstract
The prevention of age-related memory decline and dementia has been becoming a high priority because of the rapid growth in aging populations. Accumulating epidemiological and clinical studies indicate that intake of fermented dairy products rich in β-lactolin improves memory retrieval and executive function and attenuates cognitive decline in the elderly. However, the effects of long-term consumption of β-lactolin on Alzheimer’s disease (AD) pathologies have not been investigated. In the present study, we examined the effects of β-lactolin and whey digestion rich in β-lactolin on AD pathology in 5×FAD transgenic mice and PS19 tauopathy mice. Intake of β-lactolin and whey digestion rich in β-lactolin reduced the levels of inflammatory cytokines, suppressed the infiltration of activated microglia, decreased the levels of amyloid-β, ameliorated impaired long-term object memory, and attenuated decreased synaptophysin, dopamine, brain-derived neurotrophic factor, and insulin-like growth factor 1 levels in the cortex in 5×FAD transgenic mice. In addition, intake of β-lactolin and whey digestion rich in β-lactolin improved behavioral abnormality and reduced the ratio of phosphorylated tau to total tau in the cortex in PS19 tauopathy mice. These findings indicate that consumption with β-lactolin and whey digestion rich in β-lactolin suppresses inflammation and attenuates AD pathology and cognitive impairment.
Highlights
With the rapid growth in the proportions of the older population worldwide, cognitive decline and dementia are becoming an increasing burden on patients and their families and on national healthcare systems
The expressions of CD86 in CD11b-positive microglia were significantly higher in control 5 × Familial Alzheimer’s Disease (FAD) mice than in wild-type mice but were significantly lower in 5 × FAD mice fed with -lactolin and whey digestion than in control 5 × FAD mice (Fig. 2D)
Data are presented as means ± SEM. p-values shown in the graph were calculated by one-way ANOVA followed by the Tukey–Kramer test. *p < 0.05
Summary
With the rapid growth in the proportions of the older population worldwide, cognitive decline and dementia are becoming an increasing burden on patients and their families and on national healthcare systems. Because of lack of a disease therapy for dementia, preventive approaches have been receiving increasing attention. Phosphorylated tau become aggregated and are respectively deposited as senile plaques and neurofibrillary tangles (NFTs) in patients with Alzheimer’s disease (AD) [1, 2]. Accumulating evidence indicates that deposition of A and phosphorylated tau induces inflammation in the brain and exacerbates neurological deficits and cognitive decline [3,4,5]. Proliferation and activation of microglia in the brain around senile plaques and NFTs are prominent features in AD [4], and activated
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