Early Aβ-HBc virus-like particles immunization had better effects on preventing the deficit of learning and memory abilities and reducing cerebral Aβ load in PDAPP mice.

For nearly two decades, immunization against the β-amyloid peptide (Aβ) has been investigated as a potential treatment for Alzheimer's disease (AD). Despite some disappointing results in clinic trials, greater significance has been attached by some researchers to exploring the immune effects on pathological and cognitive changes in AD or producing new vaccines of AD. In the previous study, we have made a virus-like particles (Aβ-HBc VLPs) as Aβ vaccine candidate.

Ablation of aberrant neurogenesis fails to attenuate cognitive deficit of chronically epileptic mice.

Pilocarpine-induced acute seizures strongly induce aberrant hippocampal neurogenesis, characterized by increased proliferation of neural progenitors and abnormal integrations of newly generated granule cells - hilar ectopic granule cells (EGCs), mossy fibre sprouting (MFS), and hilar basal dendrites (HBDs), which may disturb hippocampal neuronal circuits and thus contribute to cognitive impairment in temporal lobe epilepsy (TLE) patients and animal models. Previous studies via ablating hippocampal neurogenesis after acute seizures produced inconsistent results regarding the development of long-term cognitive impairment. Furthermore, a sufficient decrease of subsequent abnormal integrations in chronically epileptic hippocampus was not well-established in these studies.

Reduced abnormal integration of adult-generated granule cells does not attenuate spontaneous recurrent seizures in mice.

Epileptic seizures lead to aberrant hippocampal neurogenesis, including increased proliferation of neural progenitors and abnormal integrations of newly generated granule cells - hilar ectopic granule cells (EGCs), mossy fiber sprouting (MFS), and hilar basal dendrites (HBDs). Previous results from ablating hippocampal neurogenesis after acute seizures have been controversial with regards to the development of spontaneous recurrent seizures (SRSs). While ablation of hippocampal newborn cells was effective, a sufficient decrease of subsequent abnormal integrations in chronically epileptic hippocampus was not well-established in these studies.

Maternal separation exacerbates Alzheimer's disease-like behavioral and pathological changes in adult APPswe/PS1dE9 mice.

Alzheimer's disease (AD), the most common neurodegenerative disorder that gradually destroys memory and cognitive abilities in the elderly, makes a huge emotional and economic burden on the patients and their families. The presence of senile plaques and the loss of cholinergic neurons in the brain are two neuropathological hallmarks of AD. Maternal separation (MS) is an animal paradigm designed to make early life stress.

Puerarin attenuates learning and memory impairments and inhibits oxidative stress in STZ-induced SAD mice.

Puerarin (PUE), an isoflavone purified from the root of Pueraria lobata (Chinese herb), has been reported to attenuate learning and memory impairments in the transgenic mouse model of Alzheimer's disease (AD). In the present study, we tested PUE in a sporadic AD (SAD) mouse model which was induced by the intracerebroventricular injection of streptozotocin (STZ). The mice were administrated PUE (25, 50, or 100mg/kg/d) for 28 days.

Vasoactive intestinal peptide administration after stroke in rats enhances neurogenesis and improves neurological function.

The aim of this study was to investigate the effects of vasoactive intestinal peptide (VIP) on neurogenesis and neurological function after cerebral ischemia. Rats were intracerebroventricular administered with VIP after a 2h middle cerebral artery occlusion (MCAO) and sacrificed at 7, 14 and 28 days after MCAO. Functional outcome was studied with the modified neurological severity score.

Mitogen-activated protein kinase signaling pathways promote low-density lipoprotein receptor-related protein 1-mediated internalization of beta-amyloid protein in primary cortical neurons.

Mounting evidence suggests that the pathological hallmarks of Alzheimer's disease (AD) are caused by the intraneuronal accumulation of beta-amyloid protein (Aβ). Reuptake of extracellular Aβ is believed to contribute significantly to the intraneuronal Aβ pool in the early stages of AD. Published reports have claimed that the low-density lipoprotein receptor-related protein 1 (LRP1) mediates Aβ1-42 uptake and lysosomal trafficking in GT1-7 neuronal cells and mouse embryonic fibroblast non-neuronal cells.

[Optimization of trypsin digestion intensity to obtain high-purity in vitro cultured astrocytes].

The aim of the present study was to observe the effect of trypsin digestion on the purity of in vitro cultured astrocytes and optimize the culture methods. The cerebral cortical tissue from newborn Sprague Dawley (SD) rats was isolated and digested with 0.25% trypsin for 20, 30, or 40 min.

Aβ-HBc virus-like particles immunization without additional adjuvant ameliorates the learning and memory and reduces Aβ deposit in PDAPP mice.

β-Amyloid peptide (Aβ) immunization is regarded as a promising therapy to Alzheimer's disease. The full length Aβ as antigen might induce meningoencephalitis adverse effect since the middle and C-terminal fragments of Aβ contain T cell epitopes. While N-terminal fragment of Aβ, containing B cell epitope, has weak or no immunogenicity.

Taurine attenuates amyloid β 1-42-induced mitochondrial dysfunction by activating of SIRT1 in SK-N-SH cells.

Amyloid β (Aβ) plays a critical role in the pathogenesis of Alzheimer disease (AD). Studies indicate that Aβ causes reactive oxygen species (ROS) generation, mitochondrial dysfunction and neurons loss in vivo and in vitro. Taurine, a naturally occurring β-amino acid in the brain, has been demonstrated to have neuroprotective properties.

The effects of valsartan on cognitive deficits induced by aluminum trichloride and d-galactose in mice.

Objectives: Valsartan has been reported to reduce brain beta-amyloid protein levels and improve spatial learning in the Tg2576 transgenic mouse model of Alzheimer's disease (AD). However, the exact mechanism of neuroprotective effects of valsartan has not been properly studied especially in cholinergic function and oxidative damage, the essential factors that undergo impairment in AD. Therefore, the present study examined the effects of valsartan on memory impairment, cholinergic dysfunction, and oxidative stress in aluminum trichloride (AlCl3) and d-galactose (d-gal)-induced experimental sporadic dementia of Alzheimer's type.

The effects of perindopril on cognitive impairment induced by d-galactose and aluminum trichloride via inhibition of acetylcholinesterase activity and oxidative stress.

Preclinical and clinical studies indicate involvement of renin angiotensin system (RAS) in memory functions. However, exact role of RAS in cognition is still ambiguous. The present study investigated the effects of perindopril on dementia of Alzheimer's type induced by d-galactose (d-gal) and aluminum trichloride (AlCl3).

Anti-Aβ antibodies induced by Aβ-HBc virus-like particles prevent Aβ aggregation and protect PC12 cells against toxicity of Aβ1-40.

β-Amyloid peptide (Aβ) immunization is regarded as the most promising therapy to Alzheimer' s disease. The full length Aβ as antigen might induce meningoencepholontis adverse effect since the middle and C-terminal fragments of Aβ contain T cell epitopes. While N-terminal fragment of Aβ, containing B cell epitope, has weak or no immunogenicity.

Vasoactive intestinal peptide increases VEGF expression to promote proliferation of brain vascular endothelial cells via the cAMP/PKA pathway after ischemic insult in vitro.

Vasoactive intestinal peptide (VIP) enhances angiogenesis in rats with focal cerebral ischemia. In the present study, we investigated the molecular mechanism of the proangiogenic action of VIP using an in vitro ischemic model, in which rat brain microvascular endothelial cells (RBMECs) are subjected to oxygen and glucose deprivation (OGD). Western blotting and immunocytochemistry were carried out to examine the expression of VIP receptors and vascular endothelial growth factor (VEGF) in cultured RBMECs.

[Prokaryotic expression and immunogenicity of the chimeric HBcAg containing Aβ(1-15)].

Objective: To construct a recombinant prokaryoticexpression plasmid pET/ c-Aβ(15)-c, and evaluate the immunogenicity of its encoded fusion protein as expressed in E.coli.

Methods: The gene fragment HBc88-144 was amplified by PCR and subcloned to pUC19.

Association between the apolipoprotein E4 and postoperative cognitive dysfunction in elderly patients undergoing intravenous anesthesia and inhalation anesthesia.

Background: Intravenous and inhalation anesthesia are commonly used in the clinical setting. Recovery of cognitive function in elderly patients after surgery has received increased attention. In this study, the authors compared recovery of cognitive function in patients after different anesthesia techniques, and investigated which technique is safer.

[Prokaryotic expression and immunogenicity analysis of the chimeric HBcAg containing APP beta cleavage site peptide and Aβ(1-15);].

Aim: To construct the recombinant prokaryotic expression plasmid pET/c-ABCSP-Aβ(15-c);, and evaluate the immunogenicity of the fusion protein expressed in E.coli.

Methods: The gene fragment HBc88-144 was amplified by PCR and subcloned to pUC19.

[Immunization with recombinant HBcAg and β-amyloid peptide fusion protein promotes clearance of intrahippocampally injected β-amyloid peptide in rats].

Objective: To study the effects of immunization with the fusion protein CAC (a product of prokaryotic expression of recombinant HBcAg and β-amyloid peptide fusion gene) against the toxicity induced by intrahippocampal injection of aggregated β-amyloid peptide (Aβ) in rats.

Methods: SD rats were immunized intraperitoneally with the fusion protein CAC, and the titer of anti-Aβ antibody was evaluated by ELISA. When the titers of the anti-Aβ antibody reached 1:3 000, aggregated Aβ was injected into the CA1 region of the rat hippocampus.

[Effect of [Gly14]-Humanin on Abeta(25-35)-induced PC12 cell apoptosis].

Aim: To investigate the effect of [Gly14]-Humanin overexpression on Abeta(25-35);-induced PC12 cell apoptosis.

Methods: Recombinant plasmid pcDNA3.1(-)/HNG-FLAG was transfected into PC12 cells by liposome method.

[Effect of puerarin on PC12 cells apoptosis induced by Abeta25-35 in vitro].

Objective: To establish a nerve cell injury model by incubating PC12 cell line in the presence of Abeta25-35 to study the effect of puerarin on apoptosis of nerve cells.

Methods: PC12 cells were incubated with Abeta25-35 and puerarin. Cell viability was detected by MTT.

[Biological effects of immune serum from fusion protein of beta-amyloid peptide and HbcAg/MIR on AD transgeneic cells].

Objective: To investigate the expression of fusion protein c-Abeta-c, a fusion protein from the beta amyloid peptide (Abeta) and the Hepatitis B core antigen/ Major immunodominant region (HbcAg/MIR), in the BL21/pET28 prokaryotic expression system and to immunize mice with the expressed fusion protein and evaluate the immunogenicity and biological effects of the serum in vitro.

Methods: The recombinant prokaryotic expression plasmid PET-28a /c-Abeta-c was constructed by molecular cloning technique and the c-Abeta-c fusion gene expression was induced in E. coli BL21 by isopropyl-1-thio-b-Dgalactopyranoside (IPTG).

Recombinant AAV-mediated expression of human BDNF protects neurons against cell apoptosis in Abeta-induced neuronal damage model.

The human brain-derived neurotrophic factor (hBDNF) gene was cloned by polymerase chain reaction and the recombinant adeno-associated viral vector inserted with hBDNF gene (AAV-hBDNF) was constructed. Cultured rat hippocampal neurons were treated with Abeta(25-35) and serued as the experimental Abeta-induced neuronal damage model (AD model), and the AD model was infected with AAV-hBDNF to explore neuroprotective effects of expression of BDNF. Cell viability was assayed by MTT.

Specific suppression of beta-secretase gene expression by short interfering RNA in SK-N-SH cells.

Objective: To test the effect of short interfering RNAs (siRNAs) of beta-site APP cleaving enzyme (BACE) on inhibiting the expression of BACE in mammalian cells.

Methods: The gene of EGFP, U6 promoter and beta-secretase targeting siRNA were cloned by PCR. The PCR products were inserted into the retrovirus plasmid pLXSN.