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

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) level...

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Bibliographic Details
Published in:Dementia and geriatric cognitive disorders 1999-11, Vol.10 (6), p.446-451
Main Authors: Mustafa, Amged, Lannfelt, Lars, Lilius, Lena, Islam, Atiqul, Winblad, Bengt, Adem, Abdu
Format: Article
Language:English
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
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Summary: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.
ISSN:1420-8008
1421-9824
DOI:10.1159/000017188