Magnetic nanomagnetic nanoparticles combining with Slit2 gene and bone marrow mononuclear cells to improve cognitive dysfunction in rats with chronic cerebral ischemia.

Cognitive dysfunction caused by chronic cerebral hypoperfusion (CCH) is the leading cause of vascular dementia. Therefore, it is necessary to explore the mechanism that causes cerebral injury and find an effective therapy. Bone marrow mononuclear cells (BMMNCs) were extracted to detect the activity by CCK-8 kit and verify the transfection efficiency using reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR).

Evolutionary and Expression Analysis of the Pig MAGE Gene Family.

The melanoma-associated antigen (MAGE) family found in eukaryotes plays a crucial role in cell proliferation and differentiation, spermatogenesis, neural development, etc. This study explored the validation and evolution of MAGE genes in eukaryotic genomes and their distribution and expression patterns in pigs. In total, 249 MAGE genes were found on 13 eukaryotic species.

Causal effect of the age at first birth with depression: a mendelian randomization study.

Background: This study aimed to explore the causal relationship between age at first birth (AFB) and depression.

Methods: Using the univariable Mendelian randomization (UVMR) and multivariable Mendelian randomization (MVMR) methods to examine the potential correlation between age at first birth (AFB) and major depressive disorder and postpartum depression. A public database was used to obtain the genome-wide association studies (GWAS) summary data.

Toll-like receptors (TLR2 and TLR4) antagonist mitigates the onset of cerebral small vessel disease through PI3K/Akt/GSK3β pathway in stroke-prone renovascular hypertensive rats.

To examine the effect and mechanism of Toll-Like Receptors (TLR2, TLR4) antagonist in CSVD. The rat model of stroke-induced renovascular hypertension (RHRSP) was constructed. TLR2 and TLR4 antagonist was administrated by Intracranial injection.

Epigallocatechin-3-Gallate Reduces Neuronal Apoptosis in Rats after Middle Cerebral Artery Occlusion Injury via PI3K/AKT/eNOS Signaling Pathway.

Background/aims: Epigallocatechin-3-gallate (EGCG) has neuroprotective effects and the ability to resist amyloidosis. This study observed the protective effect of EGCG against neuronal injury in rat models of middle cerebral artery occlusion (MCAO) and investigated the mechanism of action of PI3K/AKT/eNOS signaling pathway.

Methods: Rat models of permanent MCAO were established using the suture method.

Active Immunization with DNA Vaccine Reduced Cerebral Inflammation and Improved Cognitive Ability in APP/PS1 Transgenic Mice by In Vivo Electroporation.

The aggregation of amyloid β-peptide (Aβ) is thought to play a pivotal role in the disease progression of Alzheimer's disease (AD). Amyloid β directed immunotherapy has been considered an alternative AD treatment. In this study, we constructed a DNA vaccine, p(Aβ3-10)10-mIL-4, encoding ten tandem repeats of Aβ3-10 fused with mouse IL-4.

Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1-42).

Three-month-old Alzheimer's disease model transgenic mice were immunized with Aβ1-42 Plp-Adenovirus [Ad]-X-CMV-(Aβ3-10)10-CpG [AdCpG-(Aβ3-10)10] or AdCpG virus fluid via nasal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were significantly increased in mice immunized with Aβ1-42 and AdCpG-(Aβ3-10)10. Concanavalin A and AdCpG-(Aβ3-10)10 stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG(Aβ3-10)10 and Aβ42 groups compared with the control group.

A new DNA vaccine fused with the C3d-p28 induces a Th2 immune response against amyloid-beta.

To enhance anti-amyloid-beta (Aβ) antibody generation and induce a Th2 immune response, we constructed a new DNA vaccine p(Aβ3-10)10-C3d-p28.3 encoding ten repeats of Aβ3-10 and three copies of C3d-p28 as a molecular adjuvant. In this study, we administered this adjuvant cularly to female C57BL/6J mice at 8-10 weeks of age.

Reduction of cerebral Aβ burden and improvement in cognitive function in Tg-APPswe/PSEN1dE9 mice following vaccination with a multivalent Aβ3-10 DNA vaccine.

To develop a safe and efficient Aβ vaccine for Alzheimer's disease, we constructed a plasmid DNA vaccine encoding ten repeats of Aβ3-10 and three copies of C3d-p28 as a molecular adjuvant and administered it intramuscularly in 12-month-old female Tg-APPswe/PSEN1dE9 mice. Therapeutic immunization with p(Aβ3-10)10-C3d-p28.3 stimulated a Th2 immune response that elicited therapeutic levels of anti-Aβ antibodies and improved cognitive function.

In vivo electroporation of a new gene vaccine encoding ten repeats of Aβ3-10 prevents brain Aβ deposition and delays cognitive impairment in young Tg-APPswe/PSEN1dE9 mice.

Active immunization holds great promise for the treatment of Alzheimer's disease but the infiltration of T-lymphocytes and associated meningoencephalitis observed in clinical trials needs to be overcome. To avoid this toxicity, previous studies have used synthetic truncated derivatives of Aβ to promote humoral immunity. In this study, we developed a novel vaccine [p(Aβ3-10)10-MT] that expresses ten repeats of Aβ3-10 with melatonin (MT) as an adjuvant, and administered it intramuscularly in three-month-old Tg-APPswe/PSEN1dE9 (Tg) mice by in vivo electroporation.