The role of neurovascular unit damage in the occurrence and development of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disease with progressive cognitive impairment. It is the most common type of senile dementia, accounting for 65%-70% of senile dementia [Alzheimer's Association (2016). 2016 Alzheimer's disease facts and figures.

[Verification of a sporadic Alzheimer disease model in SORL1 gene knockout mice].

Objective: To compare the behavioral and pathological features of SORL1 gene knockout mice with those of normal mice and APP/PSE1 mice to verify the feasibility of using SORL1 knockout mice as a model of sporadic Alzheimer disease.

Methods: SORL1 gene of fertilized mouse eggs were edited using Crispr/Case9 technique. SORL1 mice were screened and identified by detecting the DNA sequence, and Western blotting was used to detect the expression of SORL1.

[Protective effect of butylphthalide in a cell model of Alzheimer's disease induced by Aβ25-35 in Neuro 2a cells].

Objective: To study the protective effect of butylphthalide in a cell model of Alzheimer's disease(AD) induced by Aβ25-35 in Neuro 2a (N2a) cells.

Methods: N2a cells were divided into AD group, butylphthalide (NBP) group and control group. AD cell model was established by adding 20 µmol/L Aβ25-35 to cultured N2a cells.

[Research progress of depression and the application of esketamine].

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression.

[Correlation between serum adiponectin level and cognitive function in patients with Alzheimer's disease].

Objective: To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function.

Methods: This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group.

Mutant presenilin2 promotes apoptosis through the p53/miR-34a axis in neuronal cells.

Neurodegenerative disorders have attracted attention in last decades due to their high incidence in the world. The p53/miR-34a axis triggers apoptosis and suppresses viability in multiple types of cells, but little is known about its role in neurodegenerative diseases. In this study, we showed that presenilin (PS)-2, a major gene associated with familial Alzheimer's disease (AD) could trigger the apoptosis through the p53/miR-34a axis in PC12 cells.

[Effect of willed movement therapy on GFAP and SYP expression in rats with cerebral ischemia-reperfusion].

Objective: To determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.

Methods: Adult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group.

[Effect of willed movement therapy on the expression of neurotrophin 3 and growth-associated protein 43 in rats with cerebral ischemia reperfusion].

Objective: To observe the effect of willed movement therapy on the expression of neurotrophin 3 (NT-3) and growth associated protein 43 (GAP-43) in rats with cerebral ischemia-reperfusion (IR) and investigate the neuroprotective mechanism of willed movement therapy in nerve regeneration and repair.

Methods: Cerebral IR model was established by middle cerebral artery occlusion (MCAO) in SD rats. The rats were randomly divided into MCAO group, environment modification group (EM group) and willed movement therapy group (WM group).

[Butylphthalide improves learning and memory abilities of rats with Alzheimer's disease possibly by enhancing protein disulfide isomerase and inhibiting P53 expressions].

Objective: To determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer's disease (AD).

Methods: Sixty male adult rats were randomly divided into AD model group, butylphthalide group and control group (n = 20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats.

[Effect of butylphthalide on the expression of S100 and glial fibrillary acidic protein in a rat model of Alzheimer disease].

Objective: To determine the expression of S100-beta protein and glial fibrillary acidic protein (GFAP) in hippocampal astrocytes of rats with Alzheimer disease (AD) model rats, and observe the effect of butylphthalide on their expression.

Methods: Sixty male adult rats were randomized equally into model group, butylphthalide group, and control group, and in the former two groups, AD models were established by injecting beta-amyloid protein 1-40 into the hippocampus. Sixty days later, the rats were sacrificed and the bilateral hippocampuses were taken for immunohistochemistry.

[Butylphthalide improves learning and memory abilities of rats with Alzheimer's disease possibly by inhibiting P38 mitogen-activated protein kinase and enhancing extra-cellular signal regulated kinase expressions].

Objective: To determine the effect of butylphthalide on the expressions of p38 mitogen-activated protein kinase and extra-cellular signal regulated kinases (ERKs) in the brain tissue of rats with Alzheimer's disease (AD).

Methods: Sixty male adult rats were randomly divided to AD model group, butylphthalide group, and control group (n=20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats.

Altered angiotensin-converting enzyme and its effects on the brain in a rat model of Alzheimer disease.

Background: Alzheimer disease (AD) is a neurodegenerative disease related to aging. At present, its pathological mechanisms remain unclear. Family members of the renin-angiotensin system (RAS) play a role in neuronal plasticity, as well as formation of learning and memory.

Effect of polygonum multiflorum on the fluidity of the mitochondria membrane and activity of COX in the hippocampus of rats with Abeta 1-40-induced Alzheimer's disease.

Objective: To explore the effect of polygonum multiflorum on the fluidity of mitochondria membrane and activity of cytochrome oxidase (COX) in Alzheimer's disease (AD) model rats.

Methods: Forty-five SD rats were randomly divided into 3 groups: an AD model group, a control group, and a treatment group (n=15). AD model was established by injecting beta-amyloid protein (Abeta) 1-40 into the hippocampus of rats.