根据一份报告，向经历过癫痫引发损伤的大鼠大脑注射两种小蛋白能促进损伤区域的恢复，而且可能有助于防止一种长期癫痫病的发展。已知在癫痫引发的损伤（例如长时间的抽搐）和癫痫的发展之间的这段时间会发生的进行性大脑变化，但是目前的抗癫痫药物并不能防止由这种疾病导致的大脑损伤的积累。
Michele Simonato及其同事向不致病的病毒插入了两个能促进神经元生存的小蛋白（被称为神经营养因子），从而研究减少这类大脑损伤。
尽管这两种神经营养因子都不能防止近来被长时间癫痫发作破坏的大鼠大脑细胞的死亡，这两种蛋白都能刺激大鼠大脑新神经元的生长。在进行注射之后，接受治疗的11只大鼠中的两只再也没有出现过癫痫发作，而那些确实出现了轻微癫痫的大鼠与对照组相比癫痫出现的频率和强度都更低。这组作者说，神经营养因子可能通过促进大脑受损后新神经元的生长从而减少癫痫的严重程度，而且可能用于治疗其他神经退行性疾病。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS April 6, 2009, doi: 10.1073/pnas.0810710106
Localized delivery of fibroblast growth factor–2 and brain-derived neurotrophic factor reduces spontaneous seizures in an epilepsy model
Beatrice Paradisoa,b,1, Peggy Marconib,c,1, Silvia Zucchinia,b, Elena Bertob,c, Anna Binaschib,c, Aleksandra Bozacb,c, Andrea Buzzia,b, Manuela Mazzuferia,b, Eros Magrid, Graciela Navarro Morac, Donata Rodia,b, Tao Sua,b, Ilaria Volpib,c, Lara Zanettie, Andrea Marzolad, Roberto Manservigib,c, Paolo F. Fabenee and Michele Simonatoa,b,2
aDepartment of Clinical and Experimental Medicine, Section of Pharmacology, and Neuroscience Center,
bNational Institute of Neuroscience,
cDepartment of Experimental and Diagnostic Medicine, Section of Microbiology,
dDepartment of Experimental and Diagnostic Medicine, Section of Pathology, University of Ferrara, 44100 Ferrara, Italy; and
eDepartment of Morphological and Biomedical Sciences, Section of Anatomy, University of Verona, 37129 Verona, Italy
?1B.P. and P.M. contributed equally to this work.
Abstract
A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis). Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor–2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis. It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences.
