Alzheimer and platelets: Low-density platelet populations reveal increased serotonin content in Alzheimer type dementia
2014 (English)In: Clinical Biochemistry, ISSN 0009-9120, E-ISSN 1873-2933, Vol. 47, no 15, 51-53 p.Article in journal (Refereed) Published
Introduction: Alzheimers disease (AD) is a progressive form of dementia characterized by an increase in the toxic substance beta-amyloid in the brain. Platelets display a substantial heterogeneity with respect to density. They further contain a substantial amount of beta-amyloid precursor protein. Platelets take up and store serotonin (5-HT) that plays an important role in the pathogenesis of severe depression. The current study aims to investigate platelet serotonin content in different platelet density populations. Material and methods: The study involved 8 patients (age 70 +/- 8 (SD) years) (3 females/5 males) with moderate AD. 6 healthy elderly subjects (age 66 +/- 9 (SD) years) (3 females/3 males) served as controls. The platelet population was divided into 17 subpopulations according to density, using a linear Percoll (TM) gradient. Platelets were counted in all fractions. After cell lysis an ELISA technique was employed to determine the 5-HT content in each platelet subfraction. Results: The two study groups did not differ significantly regarding platelet distribution in the gradients, but AD sufferers have a significantly higher 5-HT content (p less than 0.05) in the lighter platelet populations. Discussion: AD-type dementia proved to be associated with lighter platelets containing more 5-HT. It is possible that platelets from AD patients release less 5-HT. It is speculated that AD synapses are affected in a manner comparable to platelets, which could explain why 5-HT reuptake inhibitors are less effective in AD dementia.
Place, publisher, year, edition, pages
Elsevier, 2014. Vol. 47, no 15, 51-53 p.
Alzheimers disease; Fibrinogen; Platelets; Platelet activity; Platelet density; Platelet heterogeneity; Serotonin
Basic Medicine Clinical Medicine
IdentifiersURN: urn:nbn:se:liu:diva-111746DOI: 10.1016/j.clinbiochem.2014.07.007ISI: 000342822100008PubMedID: 25041722OAI: oai:DiVA.org:liu-111746DiVA: diva2:759794
Funding Agencies|Ahlens Foundation; Gun and Bertil Stohnes Foundation; Magnus Bergvalls Foundation; "Stiftelsen for Gamla Tjanarinnor"; Swedish Alzheimer Foundation; Swedish Board for Health and Welfare; Pfizer AB, Sweden2014-10-312014-10-312014-11-12Bibliographically approved