Cohen B M, Satlin A, Zubenko G S
Laboratory for Psychiatric Research, McLean Hospital, Belmont, MA 02178.
J Clin Psychopharmacol. 1988 Feb;8(1):43-7.
Patients with Alzheimer's disease (AD) have an apparent abnormality possibly representing an increase in the average fluidity of their cell membranes. Changes in membrane fluidity of similar magnitude to those observed in AD have been noted to lead to marked alterations in cell function. Therefore, the changes in fluidity observed in AD may be related to the symptoms of that disorder, representing either an underlying cause of dysfunction or cellular attempts to compensate for dysfunction in AD. To test these possibilities, we administered S-adenosyl-L-methionine (SAMe), an agent shown to increase membrane fluidity in animals, to patients with AD. Treatment with SAMe led to marked increases in membrane fluidity. However, it produced neither improvement nor worsening of symptoms. The results imply that while SAMe may be useful for other conditions associated with altered membrane fluidity (such as normal aging), changing membrane fluidity per se is not likely to lead to marked changes in symptoms in AD.
阿尔茨海默病(AD)患者存在明显异常,这可能表现为其细胞膜平均流动性增加。已注意到与AD中观察到的类似程度的膜流动性变化会导致细胞功能的显著改变。因此,AD中观察到的流动性变化可能与该疾病的症状相关,要么代表功能障碍的潜在原因,要么代表细胞试图补偿AD中的功能障碍。为了检验这些可能性,我们给AD患者施用了S-腺苷-L-蛋氨酸(SAMe),一种已证明能增加动物膜流动性的药物。SAMe治疗导致膜流动性显著增加。然而,它既没有改善症状,也没有使症状恶化。结果表明,虽然SAMe可能对与膜流动性改变相关的其他情况(如正常衰老)有用,但改变膜流动性本身不太可能导致AD症状的显著变化。