Blood acetyl- and butyrylcholinesterases in senile dementia of Alzheimer type

• Published in: Journal of the neurological sciences Vol. 70; no. 1; pp. 1 - 12
• Main Authors: Atack, J.R., Perry, E.K., Perry, R.H., Wilson, I.D., Bober, M.J., Blessed, G., Tomlinson, B.E.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 01.08.1985; Elsevier Science
• Subjects: Acetylcholinesterase; Acetylcholinesterase - blood; Aged; Alzheimer Disease - diagnosis; Alzheimer-type dementia; Biological and medical sciences; Butyrylcholinesterase; Butyrylcholinesterase - blood; Cholinesterases - blood; Clinical Enzyme Tests; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Depressive Disorder - diagnosis; Diagnosis, Differential; Erythrocyte; Erythrocytes - enzymology; Humans; Medical sciences; Neurology; Plasma; Erythrocyte; Plasma; Acetylcholinesterase; Butyrylcholinesterase; Alzheimer-type dementia; Cholinergic neuron; Nervous system diseases; Enzymatic activity; Alzheimer disease; Serum; Degeneration; Degenerative disease; Geriatrics
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/0022-510X(85)90182-0

The major neurochemical abnormality described to date in senile dementia of the Alzheimer type (SDAT) is a central cholinergic deficit. To determine whether this central deficit is reflected by changes in the levels of blood cholinesterases, plasma and erythrocyte acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BChE), were measured in SDAT and other psychiatric disorders. Plasma AChE, which has only recently been described in human blood, was significantly elevated ( P < 0.01) in the SDAT group compared with the control and other clinical groups investigated. In contrast there were no significant differences in the activities of either erythrocyte AChE or plasma BChE between any of the clinical groups. Although the source of plasma AChE is unknown the possibility that some portion originates from the central nervous system and that the elevated AChE levels in SDAT reflect increased release from degenerating cholinergic neurons is discussed.