内科学
痴呆
生物标志物
内分泌学
脑脊液
认知功能衰退
人口
阿尔茨海默病
糖酵解
疾病
医学
新陈代谢
生物
生物化学
环境卫生
作者
Claudio Liguori,Alessandro Stefani,Giuseppe Sancesario,Giuseppe Sancesario,Maria Grazia Marciani,Mariangela Pierantozzi
标识
DOI:10.1136/jnnp-2014-308577
摘要
We verified the occurrence of high CSF lactate levels in patients with AD, which may be ascribed to mitochondria impairment. Hypothesising that τ proteins may exert a detrimental effect on the entire cellular energy metabolism, the negative correlation found between lactate and τ-protein levels may allow speculation that τ toxicity, already demonstrated to have affected mitochondria, could also impair glycolytic metabolism with a less evident increase of lactate levels in more severe AD. Thus, we suggest a dynamic relationship between neuronal energy metabolism, τ proteins and cognitive decline in AD and propose the clinical potential of assessing CSF lactate levels in patients with AD to better define the neuronal brain metabolism damage.
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