Decreased Plasma Insulin-Like Growth Factor-I Level in Familial Alzheimer’s Disease Patients Carrying the Swedish APP 670/671 Mutation

• Published in: Dementia and geriatric cognitive disorders Vol. 10; no. 6; pp. 446 - 451
• Main Authors: Mustafa, Amged, Lannfelt, Lars, Lilius, Lena, Islam, Atiqul, Winblad, Bengt, Adem, Abdu
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.11.1999; S. Karger AG
• Subjects: Aged; Aging - blood; Alzheimer Disease - genetics; Alzheimer Disease - metabolism; Biological and medical sciences; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Heterozygote; Human Growth Hormone - blood; Human Growth Hormone - metabolism; Humans; Insulin-Like Growth Factor I - metabolism; Male; Medical sciences; Medicin och hälsovetenskap; Middle Aged; Mutation - genetics; Mutation - physiology; Neurology; Original Research Article; Prolactin - blood; Radioimmunoassay; Sweden; Sweden; Growth hormone; Insulin-like growth factor I; Prolactin; Alzheimer's disease; APP 670/671 mutation; Human; Nervous system diseases; Pathophysiology; Alzheimer disease; Family study; Somatotropin hormone; Biological marker; Insulin like growth factor 1; Cerebral disorder; Genetic disease; Blood plasma; Protein hormone; Adenohypophyseal hormone; Central nervous system disease; Degenerative disease; Hormonal investigation; Mutation; Comparative study; Quantitative analysis
• ISSN: 1420-8008; 1421-9824
• DOI: 10.1159/000017188

The plasma insulin-like growth factor I (IGF-I) level was determined in family members carrying the Swedish amyloid precursor protein (APP) 670/671 mutation with or without Alzheimer’s disease (AD) and in age-matched controls from the same family. Plasma growth hormone (GH) and prolactin (PRL) levels were also determined. Measurement of the plasma IGF-I level by radioimmunoassay revealed a significant reduction only in the family members with AD compared to age-matched controls. However, there was no significant difference in the levels of GH and PRL between the mutation carriers with or without AD and their respective age-matched controls. These findings indicate that the mechanism(s) regulating GH and PRL were preserved and those regulating IGF-I levels might be affected in AD patients with the Swedish APP 670/671 mutation.