Sodium Channel Voltage-Gated Beta 2 Plays a Vital Role in Brain Aging Associated with Synaptic Plasticity and Expression of COX5A and FGF-2.

The role of sodium channel voltage-gated beta 2 (SCN2B) in brain aging is largely unknown. The present study was therefore designed to determine the role of SCN2B in brain aging by using the senescence-accelerated mice prone 8 (SAMP8), a brain senescence-accelerated animal model, together with the SCN2B transgenic mice. The results showed that SAMP8 exhibited impaired learning and memory functions, assessed by the Morris water maze test, as early as 8 months of age.

Expressional difference, distributions of TGF-β1 in TGF-β1 knock down transgenic mouse, and its possible roles in injured spinal cord.

Transforming growth factor β1 (TGF-β1) is a multi-functional cytokine implicated in many aspects of mammalian wound healing and scar tissue formation. However, few experiments have so far addressed the potential biological effects of TGF-β1 in the nervous system after injury, in addition to the immune system. In the present study, expressional silencing TGF-β1 was achieved by selecting predesigning hairpins targeting mouse TGF-β1 genes.

Newly developed TGF-β2 knock down transgenic mouse lines express TGF-β2 differently and its distribution in multiple tissues varies.

Background: Transforming growth factor-betas (TGF-βs), including beta2 (TGF-β2), constitute a superfamily of multifunctional cytokines with important implications in morphogenesis, cell differentiation and tissue remodeling. TGF-β2 is thought to play important roles in multiple developmental processes and neuron survival. However, before we carried out these investigations, a TGF-β2 gene down-regulated transgenic animal model was needed.

miR-29c regulates BACE1 protein expression.

Recently, BACE1 expression was shown to be regulated by microRNAs, small endogenous RNA molecules that regulate protein expression through sequence-specific interaction with messenger RNA. Here, we showed that microRNA-29c (miR-29c), a miRNA that is enriched in the brain and highly expressed in the APPswe/PSΔE9 mouse lowers BACE1 protein in vitro and in transgenic miR-29c mice. In silico analysis identified two putative target sites in the BACE1 mRNA for the miR-29c family.

Evodiamine improves congnitive abilities in SAMP8 and APP(swe)/PS1(ΔE9) transgenic mouse models of Alzheimer's disease.

Aim: To investigate the effect of evodiamine (a quinolone alkaloid from the fruit of Evodia rutaecarpa) on the progression of Alzheimer's disease in SAMP8 and APP(swe)/PS1(ΔE9) transgenic mouse models.

Methods: The mice at age of 5 months were randomized into the model group, two evodiamine (50 mg·kg(-1)·d(-1) and 100 mg·kg(-1)·d(-1)) groups and an Aricept (2 mg·kg(-1)·d(-1)) group. The littermates of no-transgenic mice and senescence accelerated mouse/resistance 1 mice (SAMR1) were used as controls.