Lannfelt L, Basun H, Vigo-Pelfrey C, Wahlund L O, Winblad B, Lieberburg I, Schenk D
Karolinska Institute, Department of Clinical Neuroscience and Family Medicine, Huddinge University Hospital, Sweden.
Neurosci Lett. 1995 Oct 27;199(3):203-6. doi: 10.1016/0304-3940(95)12059-d.
The neuropathological hallmarks of Alzheimer's disease (AD) are amyloid-containing plaques and neurofibrillary tangles. The main constituent of senile plaques is amyloid beta-peptide (A beta) and in recent years, pathogenic mutations in the amyloid precursor protein (APP) gene have been discovered in some AD families. The APP670/671 mutation, found in a Swedish AD family, has revealed over-production of A beta as one pathogenic mechanism for the development of AD. In the present study we have used an immunoassay to measure A beta levels in cerebrospinal fluid (CSF) from APP670/671 mutation-carriers and non-carriers. A correlation was seen between decrease in A beta levels and duration of disease although no difference was found in levels of A beta between the groups (14.5 +/- 3.3 ng/ml versus 14.9 +/- 2.3 ng/ml).
