Adiponectin Ameliorates Cognitive Behaviors and in vivo Synaptic Plasticity Impairments in 3xTg-AD Mice.

Background: Cognitive deficit is mainly clinical characteristic of Alzheimer's disease (AD). Recent reports showed adiponectin and its analogues could reverse cognitive impairments, lower amyloid-β protein (Aβ) deposition, and exert anti-inflammatory effects in different APP/PS1 AD model mice mainly exhibiting amyloid plaque pathology. However, the potential in vivo electrophysiological mechanism of adiponectin protecting against cognitive deficits in AD and the neuroprotective effects of adiponectin on 3xTg-AD mice including both plaque and tangle pathology are still unclear.

[Expressions of synaptophysin and BDNF/Trk-B in cerebellum of APPswe/PS1dE9 transgenic mice].

Objective: To observe the expressions of synaptophysin and BDNF/Trk-B in cerebellum of APPswe/PS1dE9 transgenic mice.

Methods: The healthy 9-month old APP/PS1 male mice (n1) and the same wild type male mice(n2) were divided into two groups, APP/PS1 group and wild-type(WT) group. The expressions of synaptophysin and brain-derived neurotrophic factor/tyrosine kinase B (BDNF/Trk-B) in cerebellum were determined by Western blot (n1=6; n2=6) and immunohistochemical(n1=4; n2=4).

[Effects of adiponectin on the anxiety and memory impairment in triple transgenic Alzheimer's disease model mice].

Objective: To investigate the effects of adiponectin (APN) on anxiety and memory impairment of 9-month-old triple transgenic Alzheimer's disease (3xTg-AD) model mice.

Methods: The 9-month-old 3xTg-AD mice and C57BL/6J mice were randomly divided into four groups (=8 for each group):Wild type(WT)+Saline, 3xTg-AD +Saline, WT+APN and 3xTg-AD +APN group. All mice were implanted cannula in lateral ventricle and each mouse was intracerebroventricular injected with adiponectin or saline under free moving condition after 7 days recovery.

A novel GLP-1/GIP/Gcg triagonist reduces cognitive deficits and pathology in the 3xTg mouse model of Alzheimer's disease.

Type 2 diabetes mellitus (T2DM) is an important risk factor for Alzheimer's disease (AD). Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have been identified to be effective in T2DM treatment and neuroprotection. In this study, we further explored the effects of a novel unimolecular GLP-1/GIP/Gcg triagonist on the cognitive behavior and cerebral pathology in the 7-month-old triple transgenic mouse model of AD (3xTg-AD), and investigated its possible electrophysiological and molecular mechanisms.

[GLP-1/GIP/Gcg receptor Triagonist improves the cognitive behaviors in triple-transgenic mice of Alzheimer's disease].

Alzheimer's disease (AD) is a progressively neurodegenerative disorder, which seriously affects human health but is still irreversible up to now. Recent studies indicate that type 2 diabetes mellitus (T2DM) is an important risk factor for AD, and the drugs used for treatment of T2DM have shown some neuroprotective effects in the treatment of AD. Glucagon-like peptide-1 (GLP-1)/ glucose-dependent insulinotropic polypeptide (GIP)/glucagon (Gcg) receptor Triagonist is a new monomeric polypeptide equally activating the GLP-1/GIP/Gcg receptors, which is built on the basis of GLP-1/Gcg receptor coagonist core sequence, and incorporated with partial amino acids of GIP.

[Dual co-agonist CI-1206 antagonizes Aβ1-42-induced impairments in spatial learning and memory in mice].

Objective: To study the neuroprotective effects of a novel GIP/GLP-1 receptor dual agonist CI-1206 against Aβ1-42-induced impairments in spatial working memory and long term memory in mice.

Methods: C57 mice, after receiving intracerebralventricular (i.c.

[Role of interleukin-1 receptor antagonist in protecting kidney from injury induced by asphyxia in neonatal rats].

Objective: To observe the role of recombinant human interleukin-1 receptor antagonist (rhIL-1ra) in protecting kidney from injury induced by asphyxia in neonatal rats.

Methods: Neonatal rats were used as experimental animals. The changes in intrarenal inflammatory response and renal injury were examined in the control group (n=13), and 2, 24 and 48 hours after asphyxia followed by normal saline treatment in those treated with rhIL-1ra.