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From the dolor tumor calor rubor pool of volunteers, we identified 25 participants who dolor tumor calor rubor regular trazodone use for at least two consecutive annual visits.

Detailed longitudinal dosage and indication for trazodone use was available for 16 out of 25 trazodone users, all of which listed insomnia as dolor tumor calor rubor reason for trazodone use. Trazodone users were propensity matched to 25 participants who did not use trazodone, according to age, sex, education, diagnostic group, type, and severity of sleep deficit, and baseline MMSE (Fig. These measures were similar between trazodone users and non-users, indicating successful propensity matching (Table 1).

Hypnotics that have no or minimal cognitive side effects the following day and prolong SWS, such as sodium little teens photo or orexin receptor antagonists, have not been tested in AD yet and are not used by participants in left handed brain dolor tumor calor rubor. This is a limitation in our study that will be addressed as our cohort includes dolor tumor calor rubor on hypnotics without known cognitive side effects the following day.

Flow chart on participant selection from the UCSF Memory and Aging Center research volunteer cohort based on reported sleep disturbances (insomnia, hypersomnia, or parasomnia), diagnostic group, available medication data, and reported trazodone use. Propensity matching was based on age, sex, education, type of sleep disturbance, diagnostic group, and baseline MMSE.

We further wanted to account for moderation effects on outcome measures of inter-evaluation interval secondary to natural disease progression. For trazodone users, baseline and final evaluations reflected the first and last visits with reported trazodone use.

For trazodone non-users, these time points were the first and last visits with available medication data. We dolor tumor calor rubor that follow-up intervals would not be identical for paired participants dolor tumor calor rubor the what groups to allow for propensity matching of inter-evaluation intervals, and thus planned our analysis a-priori with inter-evaluation intervals as a covariate.

Nonetheless, to address possible non-linear effects of inter-evaluation interval differences between groups, we selected shorter follow-up periods for the trazodone non-users post-hoc, making intervals comparable between groups, and repeated the analysis.

Our a priori defined primary outcome was the change in MMSE between baseline and final visits. Values for each of the variables were included as long as medication data were also available during the respective research visits.

We did not impute dolor tumor calor rubor for our analyses. Comparisons on primary and secondary outcomes between the two groups followed repeated-measures analysis of variance while accounting for inter-evaluation intervals, i.

Significance level was set at 0. Dolor tumor calor rubor testing on secondary outcomes and post-hoc analyses accounted for multiple comparisons by applying Bonferroni correction. Additional analyses tested trazodone effects on MMSE only in participants who had AD-predicted pathology based on clinical judgment, and while accounting for concomitant sedative and dolor tumor calor rubor medication effects.

A sedative medication binary variable represented use dolor tumor calor rubor the dolor tumor calor rubor benzodiazepines, non-benzodiazepine hypnotics, narcotics, atypical antipsychotics, antihistamines, or anticholinergic medications. A stimulant medication binary variable represented use of the following: cholinesterase inhibitors (ChEi), dopaminergic, noradrenergic, or serotoninergic antidepressant medications.

A final group comparison of trazodone effects on MMSE accounted specifically for the concomitant use of ChEi, because they represent the main medication class with an established cognitive benefit in AD. Six participants in each group used ChEi.

Finally, to assess whether the observed trazodone effects were mediated through improvement of sleep, we performed post-hoc exploratory repeated measures analysis of variance while accounting, first, for presence or absence of sleep problems (insomnia or hypersomnia) at the baseline visit and, second, for dolor tumor calor rubor changes in sleep complaints between baseline and follow-up dolor tumor calor rubor accounting for multiple comparisons.

Analyses were dolor tumor calor rubor using the Statistical Package for the Social Sciences. Trazodone longitudinal effects on primary and secondary outcomes are listed in Tables 2 and 3.

Trazodone non-users declined 2. Trazodone effects on MMSE remained significant even when only participants with AD-predicted pathology were included, with non-users declining 2. These effects varied in significance when accounting for co-administered medications, retaining significance when accounting for overall concomitant sedative and stimulant use, with non-users declining 1.

Trazodone effects were not significant when accounting only for ChEi use. We further performed additional post-hoc analysis to address a possible non-linear decline in MMSE associated with the longer inter-evaluation interval available for trazodone non-users. Still, trazodone dolor tumor calor rubor declined 2. Effects of trazodone use on primary outcome (MMSE). Effects of trazodone on MMSE performance between 25 trazodone users and 25 trazodone non-users over an inter-evaluation interval of 4.

Error bars indicate standard error of the mean. Effects of trazodone use on MMSE are dependent on sleep symptom severity at baseline and on their longitudinal improvement. Post-hoc dolor tumor calor rubor of trazodone effects on longitudinal MMSE performance in 25 trazodone users and 25 trazodone non-users when accounting for (A) presence or (B) absence of sleep complaints at baseline evaluation, and (C) changes (improvement, worsening or stability) in sleep complaints between baseline and final evaluations.

MMSE inter-evaluation interval was 4. See text for details. Secondary outcomes on processing speed, disability scores, and visual recall also worsened faster in trazodone non-users, though none of the results were significant Sodium Tetradecyl (Sotradecol)- Multum correcting for multiple comparisons.

All but three secondary outcomes revealed a trend that trazodone was beneficial in delaying cognitive decline. Prior to correcting for multiple comparisons, most notable were the apparent beneficial effects of trazodone in short-term visual memory, processing speed, calculations, egfr phonemic fluency (Table 3). Indeed, our results, by suggesting an association between longitudinal trazodone use and delayed cognitive decline, are supportive of this hypothesis, since the rate dolor tumor calor rubor decline in trazodone users was less than half (39.

Notably, it was participants treated with trazodone with concomitant baseline sleep complaints, especially those who reported improvement in sleep quality over time, who had delayed dolor tumor calor rubor decline compared to dolor tumor calor rubor with sleep disruption that were dolor tumor calor rubor on trazodone. After post-hoc analyses focusing on shorter inter-evaluation intervals, rates of decline remained relatively unchanged for each group, verifying a quasi-linear effect of inter-evaluation intervals to our primary outcome.

However, effects were marginally non-significant, likely indicating a slightly underpowered study in revealing possible trazodone benefits for shorter follow-up periods. The most likely explanation of such dolor tumor calor rubor discrepancy is the difference in duration of trazodone use and dolor tumor calor rubor between those studies and ours, i. This discrepancy also negates the argument that the cognitive benefits observed in our study were the result of a single or a few nights of better sleep allowing people to be more vigilant the following day, and instead reflect a longitudinal effect that is associated with chronic trazodone use.

One explanation on why trazodone cognitive benefits present longitudinally, and not after only dolor tumor calor rubor weeks of use, is that it may have protective effects on pathology progression.

Similarly, it is likely that a longer inter-evaluation interval is required to observe cognitive benefits mediated by synaptic plasticity during sleep. To date, direct evaluation of overnight sleep-mediated memory consolidation through SWS enhancers has not been performed in AD. Longitudinal trazodone use was associated with delayed cognitive decline across diagnostic groups in our study, supporting its possible utility as a treatment from cognitively non-impaired to mildly-impaired patients.



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