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Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease caused by the complex interaction of multiple mechanisms. Recent studies examining the effect of high-fat diet (HFD) on the AD phenotype have demonstrated a significant influence on both inflammation and cognition. However, different studies on the effect of high-fat diet on AD pathology have reported conflicting conclusions. To explore the involvement of HFD in AD, we investigated phenotypic and metabolic changes in an AD mouse model in response to HFD. The results indicated there was no significant effect on Aβ levels or contextual memory due to HFD treatment. Of note, HFD did moderate neuroinflammation, despite spurring inflammation and increasing cholesterol levels in the periphery. In addition, diet affected gut microbiota symbiosis, altering the production of bacterial metabolites. HFD created a favorable microenvironment for bile acid alteration and arachidonic acid metabolism in APP/PS1 mice, which may be related to the observed improvement in LXR/PPAR expression. Our previous research demonstrated that Huanglian Jiedu decoction (HLJDD) significantly ameliorated impaired learning and memory. Furthermore, HLJDD may globally suppress inflammation and lipid accumulation to relieve cognitive impairment after HFD intervention. It was difficult to define the effect of HFD on AD progression because the results were influenced by confounding factors and biases. Although there was still obvious damage in AD mice treated with HFD, there was no deterioration and there was even a slight remission of neuroinflammation. Moreover, HLJDD represents a potential AD drug based on its anti-inflammatory and lipid-lowering effects.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the pathological hallmarks of progressive cognitive decline, extracellular accumulation of amyloid-β (Aβ) plaques and intracellular accumulation of neurofibrillary tangles
GFAP and major histocompatibility complex (MHC) class II expression were restricted to the hippocampal area in wild type mice but were overexpressed in the hippocampus and cortex of AD and AD + high-fat diet (HFD) mice
Microglial cells are first primed by intracellular accumulation of Aβ, and prior to plaque deposition, classical markers of microglial activation, such as MHC class II, inducible nitric oxide synthase, and CD40, are already upregulated in the hippocampus of transgenic mice
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the pathological hallmarks of progressive cognitive decline, extracellular accumulation of amyloid-β (Aβ) plaques and intracellular accumulation of neurofibrillary tangles. In APP knock-in mouse model, carrying a humanized Aβ sequence with the Swedish mutation (KM670/671NL), this paper shown that high fat diet treatment, despite inducing obesity and a T2DM peripheral phenotype, failed to trigger AD pathology (Salas et al, 2018). HFD had only a limited effect upon learning and memory in C57BL/6 mice despite broad peripheral changes (Mielke et al, 2006; Kesby et al, 2015). These data suggest that different modes of memory are differentially sensitive to the effects of a high-fat diet. Research on the longitudinally the effect of a high-fat diet in both control non-Tg and 3xTgAD mice found that effects on memory were transient as at the age of 11– 12 and 15–16 months no difference in time spent in the target quadrant was observed between 3xTgAD or non-Tg mice on either a control or high-fat diet (Knight et al, 2014)
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