Prevalence of cardiovascular drug use before and after diagnosis of Alzheimer's disease

2020 ◽  
Vol 300 ◽  
pp. 221-225 ◽  
Author(s):  
Mai Vu ◽  
Marjaana Koponen ◽  
Heidi Taipale ◽  
Antti Tanskanen ◽  
Jari Tiihonen ◽  
...  
Author(s):  
Sanna Vallius ◽  
Heidi Taipale ◽  
Marjaana Koponen ◽  
Anna-Maija Tolppanen ◽  
Antti Tanskanen ◽  
...  

Abstract Purpose We investigated the drug use before and after transition to automated multi-dose dispensing (MDD) service among persons with Alzheimer’s disease (AD) and compared whether the changes were similar in persons without AD. Methods The register-based Finnish nationwide MEDALZ cohort includes 70,718 community-dwelling persons diagnosed with AD during 2005–2011. Each person who initiated MDD was matched in both groups with a comparison person without MDD by age, gender and for persons with AD, also time since AD diagnosis at the start of MDD. The study cohort included 15,604 persons with AD in MDD and 15,604 no-MDD, and 5224 persons without AD in MDD and 5224 no-MDD. Point prevalence of drug use was assessed every 3 months, from 1 year before to 2 years after the start of MDD and compared between persons in MDD to those who did not have MDD. Results MDD was started on average 2.9 (SD 2.1) years after AD diagnosis. At the start of MDD, the prevalence of drug use increased especially for antipsychotics, antidepressants, opioids, paracetamol and use of ≥ 10 drugs among persons with and without AD. Prevalence of benzodiazepine use (from 12% 12 months before to 17% at start of MDD), memantine (from 29 to 46%) and ≥ 3 psychotropics (from 3.2 to 6.0%) increased among persons with AD. Decreasing trend was observed for benzodiazepine-related drugs, urinary antispasmodics and non-steroidal anti-inflammatory drugs. Conclusion MDD seems to be initiated when use of psychotropics is initiated and the number of drugs increases.


2010 ◽  
Vol 30 (11) ◽  
pp. 1883-1889 ◽  
Author(s):  
Allyson R Zazulia ◽  
Tom O Videen ◽  
John C Morris ◽  
William J Powers

Studies in transgenic mice overexpressing amyloid precursor protein (APP) demonstrate impaired autoregulation of cerebral blood flow (CBF) to changes in arterial pressure and suggest that cerebrovascular dysfunction may be critically important in the development of pathological Alzheimer's disease (AD). Given the relevance of such a finding for guiding hypertension treatment in the elderly, we assessed autoregulation in individuals with AD. Twenty persons aged 75±6 years with very mild or mild symptomatic AD (Clinical Dementia Rating 0.5 or 1.0) underwent 15O-positron emission tomography (PET) CBF measurements before and after mean arterial pressure (MAP) was lowered from 107±13 to 92±9 mm Hg with intravenous nicardipine; 11C-PIB-PET imaging and magnetic resonance imaging (MRI) were also obtained. There were no significant differences in mean CBF before and after MAP reduction in the bilateral hemispheres (−0.9±5.2 mL per 100 g per minute, P=0.4, 95% confidence interval (CI)=−3.4 to 1.5), cortical borderzones (−1.9±5.0 mL per 100 g per minute, P=0.10, 95% CI=−4.3 to 0.4), regions of T2W-MRI-defined leukoaraiosis (−0.3±4.4 mL per 100 g per minute, P=0.85, 95% CI=−3.3 to 3.9), or regions of peak 11C-PIB uptake (−2.5±7.7 mL per 100 g per minute, P=0.30, 95% CI=−7.7 to 2.7). The absence of significant change in CBF with a 10 to 15 mm Hg reduction in MAP within the normal autoregulatory range demonstrates that there is neither a generalized nor local defect of autoregulation in AD.


2008 ◽  
Vol 9 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Robin C. Fenley ◽  
Sarah J. Bober ◽  
Mebane E. Powell ◽  
Jacquelin Berman ◽  
Barbara N. Altman

This article reports on the first 2 years of an ongoing project that examined the efficacy of a 10-hour dementia training provided to entry-level personal care aide (PCA) trainees from the Hispanic, White, African American, and Asian communities in New York City. Participants were enrolled in a 90-hour PCA training program offered by the New York City Department for the Aging and were either recipients of public assistance, displaced employees from September 11, or recent immigrants to the United States from China. Classes were conducted in Spanish, English, and Mandarin/Cantonese. An 11-item Knowledge of Alzheimer’s Disease instrument was developed for the purposes of this project and administered before and after the dementia training and at 3 months following graduation. All groups, regardless of language, showed a significant increase in knowledge of Alzheimer’s disease at the conclusion of the training and retention of this knowledge at 3 months follow-up. Age was strongly correlated with an increase in knowledge, while gender and education were not.


2015 ◽  
Vol 49 (3) ◽  
pp. 809-818 ◽  
Author(s):  
Laura Saarelainen ◽  
Heidi Taipale ◽  
Marjaana Koponen ◽  
Antti Tanskanen ◽  
Anna-Maija Tolppanen ◽  
...  

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 54 ◽  
Author(s):  
Alessandro Leparulo ◽  
Mufti Mahmud ◽  
Elena Scremin ◽  
Tullio Pozzan ◽  
Stefano Vassanelli ◽  
...  

To fight Alzheimer’s disease (AD), we should know when, where, and how brain network dysfunctions initiate. In AD mouse models, relevant information can be derived from brain electrical activity. With a multi-site linear probe, we recorded local field potentials simultaneously at the posterior-parietal cortex and hippocampus of wild-type and double transgenic AD mice, under anesthesia. We focused on PS2APP (B6.152H) mice carrying both presenilin-2 (PS2) and amyloid precursor protein (APP) mutations, at three and six months of age, before and after plaque deposition respectively. To highlight defects linked to either the PS2 or APP mutation, we included in the analysis age-matched PS2.30H and APP-Swedish mice, carrying each of the mutations individually. Our study also included PSEN2−/− mice. At three months, only predeposition B6.152H mice show a reduction in the functional connectivity of slow oscillations (SO) and in the power ratio between SO and delta waves. At six months, plaque-seeding B6.152H mice undergo a worsening of the low/high frequency power imbalance and show a massive loss of cortico-hippocampal phase-amplitude coupling (PAC) between SO and higher frequencies, a feature shared with amyloid-free PS2.30H mice. We conclude that the PS2 mutation is sufficient to impair SO PAC and accelerate network dysfunctions in amyloid-accumulating mice.


2007 ◽  
Vol 3 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Rishi K. Bhalla ◽  
George D. Papandonatos ◽  
Robert A. Stern ◽  
Brian R. Ott

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