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P4–144: Treatment of agitation in people with Alzheimer's dementia: Rationale for the clinical investigation of AVP‐923 (dextromethorphan/quinidine)
Author(s) -
Schoenfeld Steven,
Tariot Pierre,
Peskind Elaine,
Cummings Jeffrey,
Lyketsos Constantine,
Nguyen Uyen,
Knowles Nadine,
Siffert Joao
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2013.05.1534
Subject(s) - dextromethorphan , memantine , pharmacology , dementia , medicine , placebo , psychology , nmda receptor , receptor , disease , alternative medicine , pathology
Background: Dementia and glaucoma have been hypothesized to be connected, through common risk factors or common mechanisms. Our aim was to evaluate the longitudinal relationship between open-angle glaucoma (OAG) and incident dementia.Methods: The 3C Bordeaux-Alienor study is a population-based cohort of 812 participants aged 72 years and over, followed-up three years. An eye examination was performed and OAG was classified according to optic nerve damage and visual field loss. Incident dementia was actively screened and confirmed by a neurologist. Results: A total of 41 participants developed a dementia over the three-year followup. Future incident dementia cases had more often a diagnosis of OAG (in 17.5% vs 4.5% for non-demented, p1⁄40.003). After adjustment for age, gender, education, family history of glaucoma, vascular comorbidities, and apolipoprotein e4, OAG participants had a nearly four-time increased risk of developing dementia over the three years of follow-up (OR1⁄43.8, 95%CI 1.5-10.1, p1⁄40.006). An increased risk of dementia was also evidenced for two markers of optic nerve degeneration (vertical cup:disc ratio and minimal rim:disc ratio) whereas no association was found between ocular hypertension and incident dementia. Conclusions: If this association between OAG and dementia is confirmed, direct and non-invasive quantification of the amount of retinal ganglion cell axonal loss might represent a useful biomarker of cerebral axonal loss in the future. It may also offer new breakthroughs in the understanding of the pathophysiological mechanisms underlying both diseases.