Cerebrospinal fluid levels of angiotensin-converting enzyme in Alzheimer's disease, Parkinson's disease and progressive supranuclear palsy

Angiotensin-Converting Enzyme Converts Amyloid β-Protein 1–42 (Aβ1–42) to Aβ1–40, and Its Inhibition Enhances Brain Aβ Deposition

“…ACE is a membrane-bound enzyme in endothelial cells and several types of epithelial and neuroepithelial cells. The active site of ACE is located in the extracellular space, and the unbound form of ACE circulating in biological fluids, such as plasma and CSF, and both types of ACE have enzymatic activity (Zubenko et al, 1985;Rigat et al, 1990;Sibony et al, 1993). These lines of evidence support our findings that ACE converts A␤ 1-42 to A␤ 1-40 and degrades A␤s under physiological conditions, thereby contributing to the prevention of A␤ deposition in the brain.…”

“…ACE activity in CSF from patients with a moderately severe senile dementia of the AD type has been shown to decrease to 41% of that in CSF from non-AD patients (Zubenko et al, 1985). Because ACE inhibitors are widely used in patients with hypertension, which is a risk factor for AD, it is important to determine the effects of ACE inhibitors on A␤ deposition in vivo.…”

Angiotensin converting enzyme and Alzheimer's disease

“…Существенное увеличение АТ 1 Р и АТ 2 Р, ассоциированное с БА, обнаружено в коре головного мозга [93,96]. Результаты изучения спинномозговой жидкости пациентов с БА, полученные различными группами исследователей, показали, что уровень АПФ либо не отличается от нормального [97,98], либо понижен по сравнению с нормой [89,92,99]. Что касается уровня АПФ кровяного русла, то имеющиеся в настоящее время данные демонстрируют как снижение уровня АПФ плазмы у пациентов с БА [100], так и его повышение [101].…”

Key Enzymes and Proteins in Amyloid-Beta Production and Clearance

“…The first correlations between ACE and AD were found in 1985 by Zubenko and colleagues (Zubenko, et al 1985) who showed that the CSF of patients with moderate degrees of senile dementia of the AD type exhibited about half the ACE activity of age and sex-matched control individuals, raising the possibility that ACE activity in the CSF could be an index of AD. In a posterior study, however, no differences in ACE activity in the CSF were found between AD patients and age matched controls raising some controversy on this issue (Konings, et al 1993), but other studies reported reduced activity of ACE in the parietal cortex of AD brains (Ichai, et al 1994).…”