科學(xué)家發(fā)現(xiàn),，當(dāng)遇到腦外傷（TBI）的小鼠食用富含支鏈氨基酸的飲食的時(shí)候,，它們比對照組小鼠的認(rèn)知恢復(fù)更好。TBI常常會(huì)破壞邊緣系統(tǒng)的海馬區(qū),，該區(qū)域參與了學(xué)習(xí)與記憶,，而且腦損傷會(huì)導(dǎo)致特定神經(jīng)元網(wǎng)絡(luò)活動(dòng)的改變，在一些區(qū)域觸發(fā)更多的活動(dòng),，而導(dǎo)致另一些區(qū)域活動(dòng)更少,。這種損傷還常常導(dǎo)致支鏈氨基酸（BCAAs）濃度的下降，BCAAs是制造基于谷氨酸的神經(jīng)遞質(zhì)（大腦通訊的媒介）的關(guān)鍵成分,。
Akiva Cohen及其同事提出,，食用BCAA可能有助于恢復(fù)被改變的神經(jīng)遞質(zhì)庫，而且可能有助于大腦在經(jīng)歷腦損傷（如那些與運(yùn)動(dòng)有關(guān)的腦震蕩帶來的損傷）之后恢復(fù)其正常功能,。這些科學(xué)家報(bào)告說,，BCAA飲食補(bǔ)充劑可能成為TBI患者的一種療法，盡管尚不清楚這種治療對于TBI在幾周或幾個(gè)月之后才顯示出來的影響是否有效,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS December 7, 2009, doi: 10.1073/pnas.0910280107
Dietary branched chain amino acids ameliorate injury-induced cognitive impairment
Jeffrey T. Colea,1, Christina M. Mitalaa, Suhali Kundua, Ajay Vermab, Jaclynn A. Elkindc, Itzhak Nissimd,e,f and Akiva S. Cohena,c,e,g,2
aDivision of Neurology
dChild Development, Children’s Hospital of Philadelphia, Philadelphia, PA 19104
bDepartment of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814
Departments of cNeurosurgery
ePediatrics
fBiochemistry and Biophysics
gNeurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104
Neurological dysfunction caused by traumatic brain injury results in profound changes in net synaptic efficacy, leading to impaired cognition. Because excitability is directly controlled by the balance of excitatory and inhibitory activity, underlying mechanisms causing these changes were investigated using lateral fluid percussion brain injury in mice. Although injury-induced shifts in net synaptic efficacy were not accompanied by changes in hippocampal glutamate and GABA levels, significant reductions were seen in the concentration of branched chain amino acids (BCAAs), which are key precursors to de novo glutamate synthesis. Dietary consumption of BCAAs restored hippocampal BCAA concentrations to normal, reversed injury-induced shifts in net synaptic efficacy, and led to reinstatement of cognitive performance after concussive brain injury. All brain-injured mice that consumed BCAAs demonstrated cognitive improvement with a simultaneous restoration in net synaptic efficacy. Posttraumatic changes in the expression of cytosolic branched chain aminotransferase, branched chain ketoacid dehydrogenase, glutamate dehydrogenase, and glutamic acid decarboxylase support a perturbation of BCAA and neurotransmitter metabolism. Ex vivo application of BCAAs to hippocampal slices from injured animals restored posttraumatic regional shifts in net synaptic efficacy as measured by field excitatory postsynaptic potentials. These results suggest that dietary BCAA intervention could promote cognitive improvement by restoring hippocampal function after a traumatic brain injury.
