是什么賦予了人類(lèi)大腦的獨(dú)特性,？在多種解釋中還尚缺髓磷脂（myelin）部分,。
傳統(tǒng)觀(guān)點(diǎn)認(rèn)為髓磷脂（Myelin）只是圍繞在神經(jīng)細(xì)胞軸突外面的一層脂質(zhì)，如同包繞電線(xiàn)的絕緣外皮,，起保護(hù)和絕緣的作用,。最近加州大學(xué)洛杉磯分校（UCLA）神經(jīng)學(xué)教授George Bartzokis博士發(fā)現(xiàn)髓磷脂問(wèn)題涉及面及廣，從精神分裂癥到阿爾茨海莫等一系列疾病都與其有關(guān),。研究結(jié)果刊登于《Biological Psychiatry》雜志,。
Bartzokis博士說(shuō)髓磷脂“進(jìn)化歷史不長(zhǎng),，脊椎動(dòng)物有而無(wú)脊椎動(dòng)物無(wú)。人類(lèi)相比于其它動(dòng)物有更多的髓磷脂,。”
Bartzokis研究報(bào)道過(guò)的類(lèi)膽堿藥（Cholinergic）的治療結(jié)果,。類(lèi)膽堿藥能夠改善阿爾茨海莫氏癥等疾病患者的神經(jīng)突觸信號(hào)傳遞。他發(fā)現(xiàn)一些臨床和理論數(shù)據(jù)提示,，這種治療有可能更改甚至推遲這些疾病,。
以髓磷脂為中心研究這種效果，Bartzokis認(rèn)為Cholinergic治療也會(huì)產(chǎn)生非突觸性效果（nonsynaptic effects）,，可能是通過(guò)增強(qiáng)髓鞘形成和髓磷脂修復(fù)——髓磷脂質(zhì)量越高,，神經(jīng)信號(hào)傳遞以及“網(wǎng)絡(luò)”（Internet）功能越好。特別是,，這種Cholinergic治療能夠增強(qiáng)少突細(xì)胞（oligodendrocytes）的活性,。少突細(xì)胞是大腦中的一種神經(jīng)膠質(zhì)細(xì)胞，在大腦發(fā)育過(guò)程中產(chǎn)生髓磷脂,，并隨著年齡增長(zhǎng)對(duì)髓磷脂起維持,、修復(fù)作用。
盡管弄清Cholinergic的非突觸性效果在大腦發(fā)育中的作用還需要做更多的工作,，但Bartzokis推測(cè)在大腦內(nèi)部進(jìn)行在體成像,，研究髓磷脂的損毀和生成，能夠輕松解決上述難題,。這些使直接在人體中檢測(cè)人腦髓磷脂中心模型的實(shí)際效用成為可能,。
“盡管這些某種程度上說(shuō)是良性干擾，”Bartzokis說(shuō)：“對(duì)大腦寶貴的少突細(xì)胞數(shù)量的影響能夠能夠抑制腦部疾病,。它們值得仔細(xì)研究,。”
英文原文：
Myelin to Blame for Many Neuropsychiatric Disorders
What makes the human brain unique? Of the many explanations that can be offered, one that doesn't come readily to mind is — myelin.
Conventional wisdom holds that myelin, the sheet of fat that coats a neuron's axon — a long fiber that conducts the neuron's electrical impulses — is akin to the wrapping around an electrical wire, protecting and fostering efficient signaling. But the research of UCLA neurology professor George Bartzokis, M.D., has already shown that myelin problems are implicated in diseases that afflict both young and old — from schizophrenia to Alzheimer's.
Now, in a report published in the journal Biological Psychiatry and available online, Bartzokis argues that the miles of myelin coating in our brain are the key "evolutionary change that defines our uniqueness as a species" and, further, may also be the cause of "our unique vulnerability to highly prevalent neuropsychiatric disorders." The paper argues that viewing the brain as a myelin-dependent "Internet" may be key to developing new and novel treatments against disease and aid in assessing the efficacy of currently available treatments, including the use of nicotine (delivered by a patch, not smoking), which may enhance the growth and maintenance of myelin.
Myelin, argues Bartzokis, who directs the UCLA Memory Disorders and Alzheimer's Disease Clinic, is "a recent invention of evolution. Vertebrates have it; invertebrates don't. And humans have more than any other species."
Bartzokis studied the reported effects of cholinergic treatments, using drugs that are known to improve a neuron's synaptic signaling in people who suffer diseases like Alzheimer's. Furthermore, he notes, some clinical and epidemiological data suggest that such treatments may modify or even delay these diseases.
Looking at such effects from a myelin-centric point of view, Bartzokis argues that cholinergic treatments may have nonsynaptic effects as well, perhaps by enhancing myelination and myelin repair — and the better the myelin, the more efficient the neuron signaling and our "Internet's" function. Specifically, such cholinergic treatments may enhance oligodendrocytes, a type of glia cell in the brain that produces myelin during the brain 's development and constantly maintains and repairs it as we age.
While more work needs to be done to fully understand the role of nonsynaptic cholinergic effects on brain development, said Bartzokis, his hypotheses can easily be tested through in vivo imaging of the brain to study the breakdown and growth of myelin. That will make it possible to directly test in humans the practical utility of the myelin-centered model of the human brain.
Ultimately, it could foster the development of novel treatments, as well as aid in assessing the efficacy of currently available treatments. These include the use of cholinergic treatments that include acetylcholinesterase inhibitors (used to treat Alzheimer's) and nicotine patches.
"Through these rather benign interventions," Bartzokis said, "such effects on the brain's vulnerable oligodendrocyte populations may offer exciting opportunities for the prevention of both developmental and degenerative brain disorders. They deserve much closer scrutiny."
Bartzokis work was supported in part by a National Institute of Mental Health grant, a National Institute on Aging Alzheimer's Disease Center Grant, Research and Psychiatry Services of the Department of Veterans Affairs and the Sidell-Kagan Foundation.
