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Amyloid-β oligomers relate to cognitive decline in Alzheimer's disease.
J Alzheimers Dis 2015; 45(1):35-43JA

Abstract

BACKGROUND

Amyloid-β (Aβ)-oligomers are neurotoxic isoforms of Aβ and are a potential diagnostic biomarker for Alzheimer's disease (AD).

OBJECTIVES

1) Analyze the potential of Aβ-oligomer concentrations in cerebrospinal fluid (CSF) to diagnose and predict progression to AD in a large clinical study sample. 2) Monitor Aβ-oligomer concentrations over-time, both in early and advanced stages of AD. 3) Examine the relation between Aβ-oligomer levels in CSF and cognitive functioning.

METHODS

24 non-demented, 61 mild cognitive impairment (MCI), and 64 AD patients who underwent lumbar puncture and cognitive testing at baseline and follow-up were selected from the memory clinic based Amsterdam Dementia Cohort. CSF samples were analyzed for standard AD-biomarkers and Aβ-oligomer levels using a validated in-house Aβ-oligomer specific enzyme-linked immunosorbent assay. Aβ-oligomer levels were analyzed as indicators of disease progression (follow-up AD diagnosis) and cognitive decline, respectively.

RESULTS

Patient groups did not differ in Aβ-oligomer concentrations at baseline or follow-up. Baseline CSF Aβ-oligomer levels were similar in MCI patients that develop AD as in stable MCI patients. MCI and AD patients showed an annual decrease in Aβ-oligomer levels of 9.4% and 6.8%, respectively. A decrease in Aβ-oligomer levels over time was strongly associated with more severe cognitive decline in AD patients.

CONCLUSION

Despite the limited diagnostic potential of Aβ-oligomer levels in CSF to differentiate between patient groups, and between MCI-AD and MCI-stable patients, changes in CSF Aβ-oligomer levels were related to cognitive decline. Therefore, CSF Aβ-oligomers may aid in the selection of patients with a more aggressive disease course.

Authors+Show Affiliations

Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands Alzheimer Center & Department of Neurology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and behaviour, Alzheimer Centre Nijmegen, Radboud University Medical Centre, Nijmegen, The Netherlands.Alzheimer Center & Department of Neurology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.Alzheimer Center & Department of Neurology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands Department of Psychiatry and Neuropsychology, Alzheimer Center Limburg, University of Maastricht, Maastricht, The Netherlands.Alzheimer Center & Department of Neurology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and behaviour, Alzheimer Centre Nijmegen, Radboud University Medical Centre, Nijmegen, The Netherlands.Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25547634

Citation

Jongbloed, Wesley, et al. "Amyloid-β Oligomers Relate to Cognitive Decline in Alzheimer's Disease." Journal of Alzheimer's Disease : JAD, vol. 45, no. 1, 2015, pp. 35-43.
Jongbloed W, Bruggink KA, Kester MI, et al. Amyloid-β oligomers relate to cognitive decline in Alzheimer's disease. J Alzheimers Dis. 2015;45(1):35-43.
Jongbloed, W., Bruggink, K. A., Kester, M. I., Visser, P. J., Scheltens, P., Blankenstein, M. A., ... Veerhuis, R. (2015). Amyloid-β oligomers relate to cognitive decline in Alzheimer's disease. Journal of Alzheimer's Disease : JAD, 45(1), pp. 35-43. doi:10.3233/JAD-142136.
Jongbloed W, et al. Amyloid-β Oligomers Relate to Cognitive Decline in Alzheimer's Disease. J Alzheimers Dis. 2015;45(1):35-43. PubMed PMID: 25547634.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Amyloid-β oligomers relate to cognitive decline in Alzheimer's disease. AU - Jongbloed,Wesley, AU - Bruggink,Kim A, AU - Kester,Maartje I, AU - Visser,Pieter-Jelle, AU - Scheltens,Philip, AU - Blankenstein,Marinus A, AU - Verbeek,Marcel M, AU - Teunissen,Charlotte E, AU - Veerhuis,Robert, PY - 2014/12/31/entrez PY - 2014/12/31/pubmed PY - 2016/3/2/medline KW - Alzheimer's disease KW - amyloid-β peptides KW - biological markers KW - cerebrospinal fluid KW - cognition KW - dementia KW - disease progression KW - mild cognitive impairment SP - 35 EP - 43 JF - Journal of Alzheimer's disease : JAD JO - J. Alzheimers Dis. VL - 45 IS - 1 N2 - BACKGROUND: Amyloid-β (Aβ)-oligomers are neurotoxic isoforms of Aβ and are a potential diagnostic biomarker for Alzheimer's disease (AD). OBJECTIVES: 1) Analyze the potential of Aβ-oligomer concentrations in cerebrospinal fluid (CSF) to diagnose and predict progression to AD in a large clinical study sample. 2) Monitor Aβ-oligomer concentrations over-time, both in early and advanced stages of AD. 3) Examine the relation between Aβ-oligomer levels in CSF and cognitive functioning. METHODS: 24 non-demented, 61 mild cognitive impairment (MCI), and 64 AD patients who underwent lumbar puncture and cognitive testing at baseline and follow-up were selected from the memory clinic based Amsterdam Dementia Cohort. CSF samples were analyzed for standard AD-biomarkers and Aβ-oligomer levels using a validated in-house Aβ-oligomer specific enzyme-linked immunosorbent assay. Aβ-oligomer levels were analyzed as indicators of disease progression (follow-up AD diagnosis) and cognitive decline, respectively. RESULTS: Patient groups did not differ in Aβ-oligomer concentrations at baseline or follow-up. Baseline CSF Aβ-oligomer levels were similar in MCI patients that develop AD as in stable MCI patients. MCI and AD patients showed an annual decrease in Aβ-oligomer levels of 9.4% and 6.8%, respectively. A decrease in Aβ-oligomer levels over time was strongly associated with more severe cognitive decline in AD patients. CONCLUSION: Despite the limited diagnostic potential of Aβ-oligomer levels in CSF to differentiate between patient groups, and between MCI-AD and MCI-stable patients, changes in CSF Aβ-oligomer levels were related to cognitive decline. Therefore, CSF Aβ-oligomers may aid in the selection of patients with a more aggressive disease course. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/25547634/Amyloid_β_oligomers_relate_to_cognitive_decline_in_Alzheimer's_disease_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-142136 DB - PRIME DP - Unbound Medicine ER -