Disease‐modifying treatments for Alzheimer's disease: A perspective based on experience with R‐Flurbiprofen

The currently available treatments for dementia caused y probable Alzheimer’s disease (AD), although beneficial o some, have proved to be of limited efficacy and are enerally considered to improve or stabilize symptoms ather than affect the underlying disease processes. There re, however, a small number of clinical studies suggesting hat cholinesterase treatments may provide a degree of neuoprotection, eg, that they may slow the progression of ippocampal (donepezil) and parietotemporal cortical (rivstigmine) atrophy, based on changes in neuroimaging paameters over time [1,2]. There is also some evidence from reclinical studies that supports the neuroprotective potenial of cholinesterase inhibitors, reviewed by Francis et al 3]. However, from a clinician’s perspective, the extent of ny neuroprotection from these drugs would seem limited, nd more effective strategies are essential. One such aproach involves R-Flurbiprofen, a potential anti-amyloid herapy, upon which this commentary is based, but there are number of others, some of which are considered elsewhere n this edition of the journal. The extensive body of evidence implicating -amyloid A ) as a potential target for disease modification strategies oes not need repeating here, nor does the epidemiologic vidence that nonsteroidal anti-inflammatory drugs NSAIDs) may have a protective effect against developing D. Early clinical trials of NSAIDs in established AD ielded disappointing results, as did a trial of prednisone, mplying that the benefits observed in epidemiologic studies ay not relate directly to anti-inflammatory activity. Evience then emerged that a subset of NSAIDs, especially urbiprofen, had the ability to selectively lower A 42 pep-