美国研究人员日前找到查出早期老年痴呆症(Alzheimer's)的方法，检验的准确率达87%。
据新加坡《联合早报》报道，另一组研究人员发现，糖尿病人患上老年痴呆症的几率较高，而且痴呆症状恶化较快。
据报道，新方法是通过测量脊髓液中的蛋白质含量，在人体出现痴呆症状和其他认知损害发生之前，就能验出疾病。宾夕法尼亚大学医学院的莱斯利·肖说：“我们可以通过新方法检查和追踪老年痴呆症的发展。”
在试验中，研究人员对410名参加大规模老年痴呆调查的病人进行了脊髓液分析。结果发现，一种名为β-淀粉样蛋白42(amyloid beta 42)的蛋白质浓度低的人，容易发展为老年痴呆症，可能是因为这种蛋白质堆积在大脑血斑中的缘故。
他们还发现，脊椎液中tau蛋白含量低的人也容易变成老年痴呆。莱斯利·肖说：“tau蛋白进入脊髓液，可能是神经细胞将要死亡时，细胞内物质释放出来造成的。”
他们的研究成果发表在《神经学年鉴》(Annals of Neurology)上。（生物谷Bioon.com）
生物谷推荐原始出处：
Annals of Neurology Volume 65 Issue 2, Pages 176 - 183
Decreased cerebrospinal fluid Aβ42 correlates with brain atrophy in cognitively normal elderly
Anne M. Fagan, PhD 1 2 3 *, Denise Head, PhD 3 4 5, Aarti R. Shah, MS 1, Daniel Marcus, PhD 4, Mark Mintun, MD 3 4, John C. Morris, MD 1 3 6, David M. Holtzman, MD 1 2 3 7
1Department of Neurology, Washington University School of Medicine, St. Louis, MO
2Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO
3Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO
4Department of Radiology, Washington University School of Medicine, St. Louis, MO
5Department of Psychology, Washington University School of Medicine, St. Louis, MO
6Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO
7Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO
Objective
For therapies for Alzheimer's disease (AD) to have the greatest impact, it will likely be necessary to treat individuals in the preclinical (presymptomatic) stage. Fluid and neuroimaging measures are being explored as possible biomarkers of AD pathology that could aid in identifying individuals in this stage to target them for clinical trials and to direct and monitor therapy. The objective of this study was to determine whether cerebrospinal fluid (CSF) biomarkers for AD suggest the presence of brain damage in the preclinical stage of AD.
Methods
We investigated the relation between structural neuroimaging measures (whole-brain volume) and levels of CSF amyloid- (A)β40, Aβ42, tau, and phosphorylated tau181 (ptau181), and plasma A40 and Aβ42 in well-characterized research subjects with very mild and mild dementia of the Alzheimer type (n = 29) and age-matched, cognitively normal control subjects (n = 69).
Results
Levels of CSF tau and ptau181, but not Aβ42, correlated inversely with whole-brain volume in very mild and mild dementia of the Alzheimer type, whereas levels of CSF Aβ42, but not tau or ptau181, were positively correlated with whole-brain volume in nondemented control subjects.
Interpretation
Reduction in CSF Aβ42, likely reflecting A aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. This suggests that there is toxicity associated with A aggregation before the onset of clinically detectable disease. Increases in CSF tau (and ptau181) are later events that correlate with further structural damage and occur with clinical onset and progression. Ann Neurol 2009;65:176-183
