van Wijk Nick, Slot Rosalinde E R, Duits Flora H, Strik Marieke, Biesheuvel Egbert, Sijben John W C, Blankenstein Marinus A, Bierau Jörgen, van der Flier Wiesje M, Scheltens Philip, Teunissen Charlotte E
Nutricia Advanced Medical Nutrition, Nutricia Research, Utrecht, The Netherlands.
Alzheimer Center and Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands.
Alzheimers Dement (Amst). 2017 May 16;8:139-146. doi: 10.1016/j.dadm.2017.04.005. eCollection 2017.
Synaptic membrane formation depends on nutrients that fuel metabolic pathways for the synthesis of constituent phospholipids. Consequently, insufficient availability of such nutrients may restrict membrane formation and contribute to synaptic dysfunction in Alzheimer's disease (AD). We assessed whether blood and cerebrospinal fluid (CSF) concentrations of nutrients related to phospholipid synthesis differ among patients with AD, mild cognitive impairment (MCI), and control subjects.
Concentrations of uridine, choline, folate, homocysteine, and other related metabolites were analyzed in paired blood and CSF samples from subjects selected from the Amsterdam Dementia Cohort with AD ( = 150; age, 66 ± 7 years; 37% female), MCI ( = 148; age, 66 ± 8 years; 37% female), and control subjects ( = 148; age, 59 ± 8 years; 38% female).
Age- and gender-adjusted analysis of variance revealed different concentrations of circulating uridine, choline, and folate and CSF uridine, folate, and homocysteine (all < .05) among the three diagnostic groups. Post hoc pairwise comparison showed that subjects with AD had lower CSF uridine, plasma choline and higher CSF homocysteine concentrations, whereas subjects with MCI had lower plasma and CSF uridine, serum and CSF folate, and higher CSF homocysteine concentrations compared with control subjects (all < .05), with differences ranging from -11 to +22%.
AD and MCI patients have lower levels of nutrients involved in phospholipid synthesis. The current observations warrant exploration of the application of nutritional strategies in the early stages of AD.
突触膜的形成依赖于为组成磷脂合成的代谢途径提供能量的营养物质。因此，此类营养物质供应不足可能会限制膜的形成，并导致阿尔茨海默病（AD）的突触功能障碍。我们评估了与磷脂合成相关的营养物质在AD患者、轻度认知障碍（MCI）患者和对照受试者中的血液和脑脊液（CSF）浓度是否存在差异。
对从阿姆斯特丹痴呆队列中选取的受试者的配对血液和脑脊液样本进行分析，这些受试者包括AD患者（n = 150；年龄，66±7岁；37%为女性）、MCI患者（n = 148；年龄，66±8岁；37%为女性）和对照受试者（n = 148；年龄，59±8岁；38%为女性）。分析尿苷、胆碱、叶酸、同型半胱氨酸及其他相关代谢物的浓度。
年龄和性别校正的方差分析显示，三个诊断组之间循环尿苷、胆碱和叶酸以及脑脊液尿苷、叶酸和同型半胱氨酸的浓度存在差异（均P <.05）。事后两两比较显示，与对照受试者相比，AD患者的脑脊液尿苷浓度较低，血浆胆碱浓度较低，脑脊液同型半胱氨酸浓度较高；而MCI患者的血浆和脑脊液尿苷浓度较低，血清和脑脊液叶酸浓度较低，脑脊液同型半胱氨酸浓度较高（均P <.05），差异范围为-11%至+22%。
AD和MCI患者参与磷脂合成的营养物质水平较低。目前的观察结果值得探索营养策略在AD早期阶段的应用。
