Rodent Study: Intranasal insulin improves cognitive deficits, ameliorates defective brain insulin signaling, strongly reduces β-amyloid (Aβ) production and plaque formation, and enhances hippocampal neurogenesis
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Let’s a take a look at a few key points from the article, shall we?
“Here, we demonstrate that intranasal insulin improves cognitive deficits, ameliorates defective brain insulin signaling, and strongly reduces β-amyloid (Aβ) production and plaque formation after 6 weeks of treatment in 4.5-month-old APPswe/PS1dE9 (APP/PS1) mice.”
“In addition, intranasal insulin effectively promotes hippocampal neurogenesis in APP/PS1 mice.”
“Intranasal insulin treatment attenuates anxiety-related behaviors and improves memory plasticity in APPswe/PS1dE9 (APP/PS1) mice.”
“Quantitative analysis revealed substantially reduced soluble Aβ oligomers in APP/PS1-ins mice (Fig. 4I), confirming that intranasal insulin can decrease Aβ levels in the brain of APP/PS1 mice.”
“Hippocampal neurogenesis plays an important role in spatial learning and memory.”
“Intranasal insulin was able to increase the number of DCX-immunoreactive cells in APP/PS1 mice (Fig. 6C), suggesting that insulin can enhance the neurogenesis in the hippocampus of APP/PS1 mice.”
“Impaired brain insulin signaling has been well documented in patients with AD and AD animal models, and has been suggested to contribute to the cognitive deficits in AD.”
“This pathological change is likely to emerge before Aβ42 accumulation.”
“It is plausible that intranasal insulin treatment can ameliorate insulin resistance due to increased IRS1pSer, leading to a reduction in Aβ production and amyloid plaque burden, and improvement of cognition.”
“Notably, soluble Aβ oligomers, which are powerful neurotoxins, were also found to decrease after insulin treatment.”
“Intranasal insulin significantly promoted neurogenesis in the brain of APP/PS1 mice.”
“IGF1 is a widely researched hormone that mediates neurogenesis (O’Kusky et al., 2000), and it is possible that intranasal insulin may enhance neurogenesis via the same mechanism as IGF1, which deserves further confirmation.”
“These findings suggest that the beneficial effects of intranasal insulin on cognition observed both in animal models and in clinical trials could at least partially be attributable to the enhancement of insulin signaling, alleviation of Aβ pathology, and promotion of neurogenesis.”
Here’s the free full text: http://onlinelibrary.wiley.com/enhanced/doi/10.1111/acel.12498/
Aging Cell. 2016 Jul 26. doi: 10.1111/acel.12498. [Epub ahead of print]
Intranasal insulin alleviates cognitive deficits and amyloid pathology in young adult APPswe/PS1dE9 mice.
Mao YF1, Guo Z1, Zheng T1, Jiang Y1, Yan Y1, Yin X1, Chen Y1, Zhang B1.
Brain insulin signaling deficits contribute to multiple pathological features of Alzheimer’s disease (AD). Although intranasal insulin has shown efficacy in patients with AD, the underlying mechanisms remain largely unillustrated. Here, we demonstrate that intranasal insulin improves cognitive deficits, ameliorates defective brain insulin signaling, and strongly reduces β-amyloid (Aβ) production and plaque formation after 6 weeks of treatment in 4.5-month-old APPswe/PS1dE9 (APP/PS1) mice. Furthermore, c-Jun N-terminal kinase activation, which plays a pivotal role in insulin resistance and AD pathologies, is significantly inhibited. The alleviation of amyloid pathology by intranasal insulin results mainly from enhanced nonamyloidogenic processing and compromised amyloidogenic processing of amyloid precursor protein (APP), and from a reduction in apolipoprotein E protein which is involved in Aβ metabolism. In addition, intranasal insulin effectively promotes hippocampal neurogenesis in APP/PS1 mice. This study, exploring the mechanisms underlying the beneficial effects of intranasal insulin on Aβ pathologies in vivo for the first time, highlights important preclinical evidence that intranasal insulin is potentially an effective therapeutic method for the prevention and treatment of AD.