Zarrouk Amira, Riedinger Jean-Marc, Ahmed Samia Hadj, Hammami Sonia, Chaabane Wafa, Debbabi Meryam, Ben Ammou Sofiene, Rouaud Olivier, Frih Mahbouba, Lizard Gérard, Hammami Mohamed
Laboratoire Nutrition, Aliments Fonctionnels et Santé Vasculaire, UR12ES05 Université de Monastir, Tunisia Equipe Biochimie du Peroxysome, Inflammation et Métabolisme Lipidique EA 7270/Université de Bourgogne/INSERM, Dijon, France.
Centre de Lutte Contre le Cancer GF Leclerc, Dijon, France.
J Alzheimers Dis. 2015;44(4):1349-59. doi: 10.3233/JAD-142046.
Several lipid metabolism alterations have been described in the brain and plasma of Alzheimer's disease (AD) patients, suggesting a relation between lipid metabolism alteration and dementia.
We attempted to identify blood fatty acids as biomarkers of dementia.
Fatty acid profiles were established using gas chromatography with or without mass spectrometry on matched plasma and red blood cells (RBCs) of demented patients diagnosed with AD, vascular dementia, or other dementia, and compared with a control group of elderly individuals. The severity of dementia was evaluated with the Mini-Mental State Examination test.
Fatty acid analysis showed significant variations of fatty acid levels in demented patients including AD patients. The highest plasma and RBC accumulation was found with hexacosanoic acid (C26:0). Our data also support that alterations of desaturase and elongase activities may contribute to cognitive dysfunction.
The variations of fatty acid levels and the accumulation of C26:0 in the plasma and RBCs highlight an alteration of fatty acid metabolism in demented patients and point toward possible peroxisomal dysfunction. It is suggested that C26:0 may constitute a convenient blood biomarker of dementia that could be useful in routine medical practice.
阿尔茨海默病（AD）患者的大脑和血浆中已发现多种脂质代谢改变，提示脂质代谢改变与痴呆之间存在关联。
我们试图确定血液脂肪酸作为痴呆的生物标志物。
采用气相色谱法（有或无质谱）对诊断为AD、血管性痴呆或其他痴呆的痴呆患者以及老年对照组的匹配血浆和红细胞（RBC）进行脂肪酸谱分析。用简易精神状态检查表评估痴呆的严重程度。
脂肪酸分析显示痴呆患者（包括AD患者）的脂肪酸水平有显著变化。发现血浆和红细胞中二十六烷酸（C26:0）的积累最高。我们的数据还支持去饱和酶和延长酶活性的改变可能导致认知功能障碍。
脂肪酸水平的变化以及血浆和红细胞中C26:0的积累突出了痴呆患者脂肪酸代谢的改变，并指向可能的过氧化物酶体功能障碍。提示C26:0可能构成一种方便的痴呆血液生物标志物，可用于常规医疗实践。
