根據(jù)一份報告，向經(jīng)歷過癲癇引發(fā)損傷的大鼠大腦注射兩種小蛋白能促進(jìn)損傷區(qū)域的恢復(fù),，而且可能有助于防止一種長期癲癇病的發(fā)展。已知在癲癇引發(fā)的損傷（例如長時間的抽搐）和癲癇的發(fā)展之間的這段時間會發(fā)生的進(jìn)行性大腦變化,，但是目前的抗癲癇藥物并不能防止由這種疾病導(dǎo)致的大腦損傷的積累,。
Michele Simonato及其同事向不致病的病毒插入了兩個能促進(jìn)神經(jīng)元生存的小蛋白（被稱為神經(jīng)營養(yǎng)因子），從而研究減少這類大腦損傷,。
盡管這兩種神經(jīng)營養(yǎng)因子都不能防止近來被長時間癲癇發(fā)作破壞的大鼠大腦細(xì)胞的死亡,，這兩種蛋白都能刺激大鼠大腦新神經(jīng)元的生長。在進(jìn)行注射之后,，接受治療的11只大鼠中的兩只再也沒有出現(xiàn)過癲癇發(fā)作,，而那些確實出現(xiàn)了輕微癲癇的大鼠與對照組相比癲癇出現(xiàn)的頻率和強度都更低。這組作者說,，神經(jīng)營養(yǎng)因子可能通過促進(jìn)大腦受損后新神經(jīng)元的生長從而減少癲癇的嚴(yán)重程度,，而且可能用于治療其他神經(jīng)退行性疾病。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
