Affiliations: [a] Department of Neuroscience and Neurology, Kuopio University, Kuopio, Finland | [b] Department of Pathology, Kuopio University Hospital, Kuopio, Finland | [c] Division of Diagnostic Services, Chromosome and DNA Laboratory, Kuopio University Hospital, Kuopio, Finland | [d] Department of Neurology, Kuopio University Hospital, Kuopio, Finland
Correspondence:
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Corresponding author: I. Alauzoff, Department of Neuroscience and Neurology and Pathology, Kuopio University, PO Box 1627, Fin 70 211 Kuopio, Finland, Tel.: +358 17 162877; Fax: +358 17 162048; E-mail: irina.alafuzoff@uku.fi
Abstract: Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAID) may have some therapeutic effect in Alzheimer's disease (AD) and experimental studies have shown that microglia activation by Aβ-peptide (Aβ) can be influenced by NSAIDs. We analysed 42 clinically and histopathologically verified demented patients fulfilling the histopathological CERAD criteria for definite AD, representing the terminal stage of brain degeneration. Our results indicate that regular NSAID use has a significant influence on the load of Aβ-peptide. Furthermore, our results indicate that regular NSAID use is associated with significantly lower counts of astrocytes and a trend of lower counts of activated microglia in the brain tissue. The influence of NSAID use was noted in all ApoE genotypes however the trend of lower counts of glial cells with regular NSAID use was more marked in patients carrying the ApoE ε4/4 alleles. Based on our results one would anticipate that regular NSAID dosing could have a beneficial effect on the progression of the disease. However, the fact that we failed to observe significant differences for activated microglia might indicate an age or stage dependent difference in the glial response i.e. in their activation rate. More studies into age and stage related factors influencing the glial response are required if one is to devise novel pharmacological treatment strategies for AD.
