CSF α₁-Antichymotrypsin and Antitrypsin in Multi-Infarct Dementia and Alzheimer’s Disease

Abstract

Alzheimer’s disease (DAT) is a degenerative disorder of the central nervous system that results in a progressive loss of memory and other intellectual functions beginning in middle to late life. Certain neuropathological lesions, such as senile plaque and neurofibrillar tangles, characterize the brains of DAT patients. Recently, two approaches — molecular cloning and immunochemical analysis — have identified one of the components of the amyloid deposits in the senile plaque of Alzheimer’s disease as the serine protease inhibitor, α₁-antichymotrypsin (ACT) [1]. In addition, the evidence of expression of ACT mRNA in astrocytes of DAT patients might support the hypothesis that ACT contributes to the pathological processes of DAT [2]. On the other hand, the cause of so-called multi-infarct dementia (MID) is believed to be ischemic insults of the brain, and the pathological findings are different from those in Alzheimer’s disease. However, because of the lack of diagnostic markers, the differential diagnosis of MID and DAT is often clinically very difficult, although Amari et al. [3] insist that there is a significant elevation of serum ACT in patients with DAT.