
Jared Saletin
· Associate Professor of Psychiatry and Human BehaviorVerifiedBrown University · Microbiology and Immunology
Active 2011–2026
About
I am an Assistant Professor of Psychiatry and Human Behavior at Brown University and the Associate Director of E.P. Bradley Hospital Sleep Research Laboratory. There, I direct the Sleep and Neurodevelopment research program. I study how sleep impacts learning and executive function in youth. We study both typically developing children and adolescents and those with significant difficulties in daytime behavior (e.g., ADHD). I utilize structural and functional MRI imaging together with topographical recordings of the sleeping EEG and field-based studies of sleep behavior. These multi-modal approaches are combined with both laboratory-based assessments of cognition and behavior (e.g., learning and memory, attention, emotion) and clinically relevant indices of dysfunction (e.g., ADHD symptomatology).
Research topics
- Medicine
- Pediatrics
- Developmental psychology
- Psychology
Selected publications
Journal of Biological Rhythms · 2026-04-06
articleOpen accessSenior authorAdolescents experience chronic sleep restriction and developmental changes in circadian biology. Sleep aids adolescent learning and memory; the moderating effect of circadian rhythms is largely unknown. Here we examine adolescent sleep restriction, circadian biology, and memory consolidation. Adolescents were recruited for a larger experimental study. This study includes a subsample of individuals from the larger study who completed the motor sequence task (MST; added toward the end of data collection). Participants ( M AGE = 12.7, SD = 1.8; 62.5% male) completed a self-selected 9 h in bed sleep stabilization schedule for 19 nights followed by 7 nights of sleep restriction (6 h in bed; bedtime delayed and risetime advanced equally). In-lab dim light melatonin onset (DLMO) was assessed on the final nights of stabilization and restriction. The MST indexed overnight memory consolidation across the final night of sleep restriction. MST outcomes included the average number of correct sequences per trial, # of errors, and precision. We examined overnight improvement (morning-evening) in MST performance and associations between improvement, phase preference, DLMO Stabilization , DLMO Restriction , and DLMO Shift (DLMO Stabilization − DLMO Restriction ), controlling for age where statistically justified. The average number of correct sequences per MST trial improved, t (15) = −3.44, p < 0.01, d = 0.86, for the morning (12.94 ± 6.89) test session compared to evening (10.81 ± 5.69). There were no changes in errors or precision ( d s < 0.14, p s > 0.34). Greater delays in DLMO phase ( M ± SD : 10.34 ± 41.69 min) were associated with greater overnight improvement in the average number of correct sequences per trial, Adj. R 2 = 0.54, F (2, 13) = 9.79, p < 0.01, and errors, Adj. R 2 = 0.21, F (1, 15) = 4.94, p < 0.05. Overnight improvement was not related to phase preference (Adj. R 2 s < 0.17; p s > 0.05). These data highlight context dependent benefits of sleep for adolescent memory consolidation and indicate a potential link between circadian biology and the cognitive benefits of adolescent sleep. Understanding the influence of circadian rhythms in sleep-dependent memory may inform discussions of adolescent sleep loss and learning.
Adolescent sleep: a bulwark for healthy brain development
SLEEP · 2026-03-21
articleSenior authorAutism Research · 2025-05-06 · 1 citations
articleOpen accessABSTRACT Autistic children often consume less varied diets, experience sleep difficulties, and have higher rates of mental health problems as compared to neurotypical peers. Yet, the direct relationship between all of these domains is not well characterized. We leveraged the Adolescent Brain Cognitive Development SM study (ABCD study) dataset to explore whether estimated levels of consumption of specific macro‐ and micronutrients correlated with the severity of mental health and sleep problems in autistic youth. We found that low vitamin B3, B6, C, and iron intake was associated with more severe psychiatric problems in autistic children in the ABCD cohort, though these findings did not reach statistical significance after correction for multiple comparisons. In a post hoc analysis, we found that the severity of sleep difficulties was correlated with estimated levels of Vitamins B3, B6, C, and iron intake and with the severity of anxiety/depressive symptoms and/or thought problems. Our analysis on a large number of nutrients, psychiatric symptoms, and sleep serves as an exploratory, initial analysis to identify specific nutrients and psychiatric symptoms that could be the focus of future (confirmatory) studies on the relationship between nutrition, sleep, and mental health in autistic individuals.
SLEEP · 2025-05-01
articleOpen accessAbstract Introduction 22q11.2 Deletion Syndrome (22q11DS) is a recurrent copy number variant with a wide range of impacts on neurodevelopment. Sleep disturbances are common among 22q11DS, a population at greatly elevated risk for psychosis. Prior studies in 22q11DS report a positive association between psychosis-risk symptoms and sleep disturbances. However, these findings are limited by the use of a single sleep rating from a structured clinical interview. Here, we use an objective sleep measure, wrist actigraphy, to examine whether psychosis-risk symptoms are related to sleep duration and wake after sleep onset (WASO) in 22q11DS. Methods 22q11DS participants (n=25 [10 male], Mage=17.1±7.3 years) and typically developing (TD) controls (n= 26 [12 male], Mage=18.3±5.4 years) completed approximately one week of actigraphy (Axivity AX6). Average sleep duration and WASO were derived from accelerometer data processed using the vanHees 2018 algorithm implemented using the GGIR R package. A clinical assessment of psychosis-risk symptoms (Structured Interview of Psychosis-Risk Syndromes; SIPS) gave indices of positive, negative, and disorganized symptom severity. Using linear regression, we tested a group-by-sleep interaction to determine if the relationship between symptoms and sleep differed between groups. If there was no significant interaction, we reported the effect of sleep on symptoms across groups. Age and sex were included as covariates in all models. Results 22q11DS participants exhibited increased sleep duration (m±sd: 7.6±1.0 hours) compared to TD participants (m±sd: 6.9±0.9 hours; b=-0.70, p=0.011). They demonstrated more severe negative symptoms compared to controls (b=-0.77, p=0.006), but there was no significant difference between groups in positive (b=-0.33, p=0.228) and disorganized symptoms (b=-0.51, p=0.057). Across groups, increased sleep duration was associated with increased positive (b=0.31, p=0.049) and disorganized symptoms (b=0.34, p=0.028). Group did not moderate the association between sleep duration and positive or disorganized symptoms. There were no other significant relationships between sleep and psychosis-risk symptoms (all p’s&gt;0.083). Conclusion 22q11DS participants exhibited increased sleep duration and negative symptoms. Our findings support prior research reporting associations between sleep and psychosis-risk symptoms. Future research utilizing measures of sleep neurophysiology is required to further understand the mechanistic relationship between sleep and psychosis-risk. Support (if any) R01MH085953; Autism Speaks Pre-Doctoral Fellowship; UCLA Center for Autism Research and Treatment Pilot Grant
0266 Sleep Restriction, Academic-Oriented Performance, and ADHD Severity in Adolescents
SLEEP · 2025-05-01
articleOpen accessSenior authorAbstract Introduction Adolescents experience insufficient sleep that may impact academic performance. Youth with attention-deficit/hyperactivity-disorder (ADHD) may be particularly vulnerable to the effects of sleep loss. By leveraging ecologically relevant tests of math and language arts, we investigated how sleep restriction affects academic performance in children differing in ADHD symptoms. Methods Fifty-seven adolescents from R01HD103665 provided usable data (27M; age: 11.6±1.04yrs, range: 10-15yrs) and were grouped by ADHD symptoms on the Conners-3-Parent ADHD Index Probability score as high (ADHDy; ≥50%ile; n=25) or low (ADHDn; &lt; 50%ile; n=32). All completed online quizzes featuring standardized-test math and language questions (prior grade-level) during two counterbalanced conditions: 5 nights of sleep optimization (10h TIB) and 5 nights of sleep restriction (7.5h TIB, equally delaying bedtime and advancing risetime). Quizzes were given in the afternoon after 1, 3, and 5 nights of each condition graded from 0-8 correct answers. We examined performance on days 1 and 5 and the change from day 1 to 5. All analyses used 2x2 ANOVAs modeling effects of group (ADHDy vs. ADHDn) and condition (restriction vs. optimization). Results For performance on Days 1 and 5, we found no significant main effects or interactions (all p’s&gt;=.09, ηp²’s=&lt;.07), and a trending main-effect of group at Day 1. With respect to change in performance (Day 5 - Day 1), we found a significant main-effect of condition (F(1,41)=4.30, p=.04, ηp²=.09), such change in performance during the restriction condition (0.68±0.24 points) was higher overall than during the optimization condition (-0.03±0.3 points), and a trending main-effect of group (F(1,41)=3.73, p=.06, ηp²=.08), but no condition-x-group interaction (F(1,41)=0.01; p=.92; ηp²=.00). Post-hoc tests indicated performance in the ADHDy group increased from Day 1 to 5 during sleep restriction (1.10±1.58 points; t(20)=-3.18; p=.01; d=1.58) but not during sleep optimization (.09±2.24 points; t(22)=-0.19; p=.85; d=-.039). ADHDn group performance did not change across either condition (p’s &gt;.23). Conclusion These analyses examine whether ADHD symptoms moderate the impact of 5-nights of insufficient sleep on academic performance. We identify paradoxical improvements across sleep restriction but only in youth with high ADHD symptoms. We will next examine how compensatory factors such as hypervigilance may explain these results. Support (if any) R01HD103655 (JMS); P20GM139743 (MAC).
2025-09-11
preprintOpen accessStudy Objectives: 1. To investigate the effect of Cognitive-behavioral therapy for insomnia (CBT-I) on memory performance and slow-wave activity (SWA) in older adults with insomnia disorder. 2. To determine whether changes in SWA are linked to improvements in memory performance. 3. To assess how the individual therapies of CBT-I treatment contribute to these effects. Methods: A secondary analysis was conducted using data from 104 older adults with insomnia disorder enrolled in a clinical trial examining the impact of CBT-I, Behavioral Therapy (BT), and Cognitive Therapy (CT) on insomnia severity. Participants were randomized to six sessions of BT, CT, or CBT-I (combined BT and CT). They underwent polysomnography and RBANS memory testing ––assessing immediate (List Learning and Story Memory) and delayed memory (List Recall, Story Recall, Figure Recall, and List Recognition)–– at baseline and at 6-month follow-up. Linear-mixed effects models examined the impact of treatment on memory and SWA. Regression analyses examined relationships between changes in SWA and memory following the treatment. Results: Improvements were identified in immediate memory (List Learning and Story Memory) and delayed memory (List Recall, Story Recall, and Figure Recall). The analysis did not reveal significant changes in SWA following treatment. However, there was a significant positive association between improvements in List Learning and increases in SWA. There were no differences in outcomes among the treatments. Conclusions: These findings suggest that BT, CT and CBT-I may enhance memory performance in older adults with insomnia disorder, with a potential link between SWA and immediate memory performance.
SLEEP · 2025-05-01
articleOpen accessSenior authorAbstract Introduction Sleep restriction compromises vigilance. While adolescents commonly experience sleep loss, attention-deficit/hyperactivity disorder (ADHD) may expose vulnerability. Reaction time variability (RTV) is a cardinal deficit of ADHD, yet it is relatively understudied as a sleep loss phenotype compared to lapses. As vigilance may further contribute to mental health in ADHD, we investigated how ADHD and mental health symptoms interact with the effect of sleep restriction on vigilance and response time variability in youth. Methods Fifty-five adolescents in R01HD103665 (29F; ages: 12.3±1.2yrs, range: 10-15yrs) completed two crossover conditions: sleep optimization (5 nights of 10h time-in-bed (TIB) anchored to optimal risetimes) and sleep restriction (5 nights at 7.5h TIB; equally delaying bedtime and advancing risetime). After each condition, participants completed a 10-minute psychomotor vigilance task (PVT) yielding lapse (RTs&gt;500ms) and reciprocal reaction time (1/RT [RRT]) variables. We then separated gaussian and exponential components of the RT distribution and estimated RTV via sigma (gaussian variability) together with mu and tau (means of gaussian and exponential components). Conners-3 parent t-scores indexed ADHD symptoms in inattention (58.0±14.0; range: 40-90) and hyperactivity/impulsivity (60.6±16.4; range: 41-90) domains. Mental health symptoms were measured on PROMIS scales for child-reported anxiety (47.8±9.0; range: 35.6-66.2) and anger (45.1±8.9; range: 31.5-61.6) and psychological stress (parent-report 47.8±14.9; range: 4-71.1; child-report: 50.1±8.1; range: 39.5-68.8). Separate linear mixed models examined how sleep condition (restriction vs. optimization) and each symptom interact in explaining PVT performance. Results Sleep restriction moderated the effect of inattention on RTV (b=0.51, SE=0.24, p=.042). Higher inattention was associated with more variable RTs (sigma) only in sleep restriction. For lapses, we identified a main-effect of condition (b=12.68, SE=4.74, p=.010) and an interaction with psychological stress (b=-0.21, SE=0.095, p=.032); worse psychological stress was associated with fewer lapses after sleep restriction. No other analyses were statistically significant. Conclusion These data indicate that ADHD and mental health symptoms may differentiate vigilance and response time variability after sleep restriction. The well-established association between ADHD symptoms and response time variability was only observed in sleep restriction; optimizing sleep schedules may mask ADHD sequelae. We will continue to probe the origin and consequence of these inter-individual differences. Support (if any) R01HD103655 (JMS); P20GM139743 (MAC).
SLEEP · 2025-05-01
articleOpen accessAbstract Introduction 22q11.2 deletion (22qDel) is a recurrent copy number variant that greatly increases risk for Schizophrenia and is associated with lower IQ. Recent work by our group has shown diminished sleep dependent memory consolidation (SDMC) in 22qDel carriers, but it is unclear whether this is associated with sleep spindle dysfunction, nor whether sleep spindles are associated with IQ, as in idiopathic schizophrenia. Methods 22qDel carriers (n=20, Mage=20.1±6.1, 10F) and typically developing (TD) controls (n=19; Mage=18.8±3.8, 12F) completed multiple nights (149 nights total; 1-8 nights per subject; median=3 nights) of sleep EEG recordings with a wearable headband (Dreem 3), along with the Wechsler Abbreviated Scale of Intelligence (WASI-II), and a motor sequence SDMC task. Unique sleep spindles were detected across a wide frequency range (10-16Hz) from the F8-F7 derivation during non-rapid eye movement sleep using Luna. We examined group differences in spindle density at each frequency (0.5Hz bins) using linear mixed effects models, accounting for multiple nights’ data. We examined if spindle properties averaged across nights (amplitude, density, duration) were related to individual differences in cognition (SDMC, IQ) within group, and whether group moderated such effects. All models controlled for age and sex. Results 22qDel Carriers exhibited an altered frequency distribution of sleep spindles, with a peak frequency of 12.5 Hz, compared to the TD group (peak at 11.5 Hz). Spindle density was significantly different between groups at 12.5Hz (b= -0.55, p= 0.02). No group differences in spindle amplitude or duration were detected at this 12.5 Hz target frequency (p’s &gt; 0.77). Group moderated (b=-1.7, p=0.05) an association between spindle amplitude and SDMC, such that smaller spindle amplitude was associated with better SDMC in controls (b=-2.03, p&lt; 0.01) but not 22qDel carriers (b=-0.34, p=0.49). Unexpectedly, there were no significant relationships between any spindle metric and IQ (all p’s &gt;0.14). Conclusion These results indicate 22qDel carriers exhibit differences in the intrinsic frequency and functional outcomes of frontal sleep spindles. These differences may reflect underlying differences in thalamocortical circuitry. Our future work will include investigating the relationship between SDMC and spindle-slow oscillation coupling. Support (if any) R01MH085953; Autism Speaks Pre-Doctoral Fellowship; UCLA Center for Autism Research and Treatment Pilot Grant
0027 Success of At-Home Dim Light Melatonin Onset Assessment in Early Adolescents with ADHD Symptoms
SLEEP · 2025-05-01
articleOpen accessSenior authorAbstract Introduction Circadian rhythms may be translationally relevant to adolescents with attention-deficit/hyperactivity-disorder (ADHD). Laboratory assessment of dim-light-melatonin-onset (DLMO) can be burdensome and prohibitive in youth with more severe ADHD presentations. Conversely, at-home protocols, while beneficial, may be impacted by the heterogeneity of ADHD. Here we examined the success of an at-home DLMO protocol in adolescents with lesser and greater ADHD severity. Methods Sixty adolescents (28M; age: 11.76±1.24 years, age-range: 10-15 years) in R01HD103665 ranging in ADHD presentation completed at least five nights of a fixed sleep schedule (10hr fixed to family-optimal rise time) followed by an evening DLMO assessment. Each was provided a collection kit including instructions, salivettes (Sarstedt AG & Co. KG), a 0.1-gram scale, log, ice pack, and light-blocking glasses. On the evening of assessment, staff described procedures over a video call and youth provided 10 saliva samples over 4.5hrs extending 1-hour past scheduled bedtime. Saliva was collected using salivettes and weighed by participants (targeting 9g; a second sample requested if weight&lt; 8.7g). Staff called participants every 30 minutes to prompt sampling, and to log start and end-times and sample weight. Samples were stored in an insulated bag with an ice-pack and retrieved the next morning. Melatonin was measured by radioimmunoassay. DLMO phase was computed by interpolation (absolute threshold of 4 pg/ml). Indeterminate DLMO phases were resolved via consensus. We examined success of DLMO determination and whether it varied by ADHD symptoms (participants grouped by Conners-3-Parent ADHD Index Probability score as high (ADHDy; ≥50%ile; n=28) or low (ADHDn; &lt; 50%ile n=32)). Results DLMO determination was successful in 92% of youth (n=55); five participants’ data required adjudication (e.g., interpolation between two threshold crossings). We failed to identify DLMO in 5 participants (8%) for persistent suprathreshold melatonin values (n=3) or measurement error (n=2). ADHD status did not moderate measurement success (χ2=0.69, p=.44, Cramer’s V=0.16). DLMO was identified in 96% of the ADHDy group (n=27) and 87% of the ADHDn group (n=28). Conclusion This work indicates the success of capturing at-home melatonin onset phase in our young sample on a fixed sleep schedule. ADHD status did not moderate the success of measurement. Support (if any) R01HD103655 (JMS); P20GM139743 (MAC)
SLEEP · 2025-04-03 · 2 citations
articleOpen access1st authorCorresponding
Recent grants
Frequent coauthors
- 129 shared
Mary A. Carskadon
Brown University
- 50 shared
Daniel P. Dickstein
- 38 shared
Sarah M. Honaker
Indiana University
- 37 shared
David Barker
Providence College
- 35 shared
M. Elisabeth Koopman‐Verhoeff
Harvard University
- 31 shared
Matthew P. Walker
University of California, Berkeley
- 30 shared
Judith Owens
Harvard University
- 30 shared
Lisa J. Meltzer
National Jewish Health
Labs
Education
Postdoctoral Research Fellow, Psychiatry and Human Behavior
Brown University Warren Alpert Medical School
- 2014
PhD, Psychology
University of California Berkeley
- 2008
BA, Psychological and Brain Sciences
Johns Hopkins University
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