The therapeutic effect of vaccination on neuronal change in animal models with Alzheimer disease

最近有报道称，将淀粉样蛋白(疫苗)注射到PDAPD鼠体内可显著减少淀粉样斑块沉积，尽管目前尚不确定淀粉样斑块是否是阿尔茨海默病的真正原因。将淀粉样蛋白β多肽注射到Niemann-Pick病C型小鼠和唐氏综合征小鼠的动物模型中，因为无论这种疫苗接种是否影响脑组织的APD值和神经原纤维的变化，APD值本身就是阿尔茨海默病的病因，疫苗是一种有效的治疗方法。NPC-SPM小鼠与NPC-NIH小鼠的病理差异不大，但NIH小鼠的寿命较短。然后每两周给SPM小鼠接种一次疫苗。其临床表现和生存期与未接种疫苗的小鼠无明显差异。在神经学上，接种疫苗的小鼠的星形胶质细胞反应受到轻微影响。为了评价长程免疫效果，对Dn小鼠进行了长达10个月的免疫(8个月免疫)。大脑皮层和海马区的神经萎缩从4月龄小鼠逐渐发展到10月龄小鼠。10月龄小鼠苍白球内可见钙化，基底前脑可见胶质细胞增生。而GFAP染色的脑白质皮质下胶质细胞增生较轻。

It has recently been reported that amyloid injection (vaccine) into PDAPD mice resulted in marked decrease of amyloid plaque deposition (APD), although it is uncertain whether or not amyloid plaque is the real cause of Alzheimer disease. Amyloid- β -peptide injection into animal models of Niemann-Pick disease type C (NPC) mice (spm, NIH) and Down syndrome (Dn) mice was projected in that whether or not such vaccination effects the brain tissue with APD and neurofibril change, APD itself is responsible for Alzheimer's etiology, and vaccine is an effective therapy. The pathological difference is only slight between NPC-spm and NPC-NIH mice, but the life span is shorter in NIH mice. We then vaccinated spm mice every 2 weeks. The clinical manifestation and life span were not different from non-vaccined mice. Neurologically, glial reaction of astrocytea was slightly affected in vaccinated mice. To evaluate the long span effect, Dn mice were vaccinated up to 10 months (8 month vaccination). Neural atrophy in cerebral cortex and hippocampus was progressive from 4 -month-old mouse to 10 -month-old mouse. Ten- month-old mouse showed calcification in pallidum and gliosis in basal forebrain. However, gliosis in cerebral subcortex of white matter, stained with GFAP was milder.