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Elevated cerebrospinal fluid BACE1 activity in incipient Alzheimer disease.

Artikel i vetenskaplig tidskrift
Författare Henrik Zetterberg
Ulf Andreasson
Oskar Hansson
Guoxin Wu
Sethu Sankaranarayanan
Malin E Andersson
Peder Buchhave
Elisabet Londos
Robert M Umek
Lennart Minthon
Adam J Simon
Kaj Blennow
Publicerad i Archives of neurology
Volym 65
Nummer/häfte 8
Sidor 1102-7
ISSN 1538-3687
Publiceringsår 2008
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 1102-7
Språk en
Länkar dx.doi.org/10.1001/archneur.65.8.11...
Ämnesord Aged, Aged, 80 and over, Alzheimer Disease, cerebrospinal fluid, enzymology, pathology, Amyloid, adverse effects, physiology, Amyloid Precursor Protein Secretases, cerebrospinal fluid, physiology, Aspartic Endopeptidases, cerebrospinal fluid, physiology, Axons, enzymology, pathology, Biological Markers, cerebrospinal fluid, Case-Control Studies, Enzyme Activation, physiology, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Middle Aged, Nerve Degeneration, cerebrospinal fluid, enzymology, pathology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

BACKGROUND: We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD). OBJECTIVE: To assess CSF BACE1 activity in AD. DESIGN: Case-control and longitudinal follow-up study. SETTING: Specialized memory clinic. Patients Eighty-seven subjects with AD, 33 cognitively normal control subjects, and 113 subjects with mild cognitive impairment (MCI), who were followed up for 3 to 6 years. MAIN OUTCOME MEASURES: Cerebrospinal fluid BACE1 activity in relation to diagnosis and CSF levels of secreted APP and amyloid beta protein (Abeta) isoforms and the axonal degeneration marker total tau. RESULTS: Subjects with AD had higher CSF BACE1 activity (median, 30 pM [range, 11-96 pM]) than controls (median, 23 pM [range, 8-43 pM]) (P =.02). Subjects with MCI who progressed to AD during the follow-up period had higher baseline BACE1 activity (median, 35 pM [range, 18-71 pM]) than subjects with MCI who remained stable (median, 29 pM [range, 14-83 pM]) (P < .001) and subjects with MCI who developed other forms of dementia (median, 20 pM [range, 10-56 pM]) (P <.001). BACE1 activity correlated positively with CSF levels of secreted APP isoforms and Abeta(40) in the AD and control groups and in all MCI subgroups (P < .05) except the MCI subgroup that developed AD. Strong positive correlations were found between CSF BACE1 activity and total tau levels in all MCI subgroups (r >or= 0.57, P

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