About

Steven T DeKosky is a prominent researcher in Alzheimer’s disease and traumatic brain injury, serving as the Deputy Director of the McKnight Brain Institute and a Professor of Neurology and Neuroscience at the University of Florida. He joined UF in July 2015 and has a distinguished background that includes roles such as vice president and dean of the University of Virginia School of Medicine, as well as chair of the department of neurology and director of the Alzheimer’s Disease Research Center at the University of Pittsburgh. His research focuses on understanding the neurochemistry, neuroimaging, treatment, and prevention of Alzheimer’s disease, with extensive contributions to the study of traumatic brain injury, including co-authoring the first report of dementia associated with TBI among professional football players. Dr. DeKosky completed his medical degree at the University of Florida, followed by a residency in neurology and a fellowship in neurochemistry, and has held academic and leadership positions at several prestigious institutions.

Research topics

• Medicine
• Psychology
• Neuroscience
• Computer Science
• Pathology
• Biology
• Pediatrics
• Intensive care medicine
• Clinical psychology
• Psychiatry
• Molecular biology
• Cognitive psychology
• Internal medicine
• Biochemistry
• Bioinformatics
• Psychotherapist
• Chemistry

Selected publications

• Pain and Nutrition in Dementia and Alzheimer’s Phase 1: a cross-sectional, observational study design

  Frontiers in Dementia · 2026-03-31

  articleOpen access

  Background: Neurodegenerative diseases such as Alzheimer's Disease and related dementias (ADRDs) as well as chronic pain have increased in prevalence as the population ages. In fact, recent epidemiological research suggests that having chronic pain may increase one's risk of all-cause dementia. There are mechanistic factors that overlap in both ADRD and chronic pain progression, including epigenetic dysregulation that could lead to increased inflammation. Previously, our group presented evidence that dietary patterns impact inflammatory potential and epigenetic modifications, and accelerate epigenetic aging. Here, we hypothesize that diet- induced inflammation and epigenetic alterations may be underexplored mechanistic pathways connecting chronic pain and ADRD risk. Methods: The Pain and Nutrition in Dementia and Alzheimer's Phase 1 (PANDA-1) study is a cross-sectional, observational study, which will recruit 90 individuals ≥55 years of age with and without painful knee osteoarthritis (OA). Biological samples will be collected to assess study eligibility, blood-based inflammatory markers, and epigenetic age using the epigenetic clock DNAmGrimAge. A 24-h dietary recall will be completed to determine nutrition status via the Dietary Inflammation Index (DII). Pain and psychosocial questionnaires will be employed to determine pain phenotypes. Quantitative Sensory Testing will be conducted to determine responses to noxious mechanical and thermal stimuli. Lower-extremity function and mobility measures will also be obtained. Finally, height, weight, pain history, medical history, medication use, and demographic variables will be collected as covariates. Hierarchical regression, mediation and moderation analyses, as well as ANOVAs will be conducted to evaluate relationships among the DII, epigenetic aging, cognition status, and pain. Conclusion: This study will integrate dietary, epigenetic, and cognitive assessments in a chronic pain population, to lay the groundwork of a possible associations linking chronic pain and ADRDs. PANDA-1 aims to determine potential relationships of dietary patterns on interindividual variability of cognitive status and pain outcomes in older adults deemed cognitively intact. Subsequent phases of this study will include individuals with mild cognitive impairment and ADRDs. Findings from this work will inform future studies targeting dietary intervention approaches to mitigate overlapping neurodegenerative and pain-related aging processes.

  PublisherOA PDFDOI

• Preoperative Visual Attention, Postoperative Delirium and Three‐Month Outcomes

  Alzheimer s & Dementia · 2025-12-01

  articleOpen access

  BACKGROUND: Preexisting cognitive impairment is a significant risk factor for post operative delirium (POD), and POD increases morbidity and mortality. Disturbances of attention and awareness are necessary for delirium diagnosis, suggesting dysfunction in frontoparietal networks, which control visuospatial attention. However, preoperative visual attention has not been systematically investigated as a risk factor for delirium and adverse longitudinal outcomes in at-risk adults. We provide an update from the study "Visual Attention and Postoperative Delirium" (AACSF-22-928731). METHODS: In this prospective observational study, participants aged 65 years and older undergoing elective orthopedic surgery completed preoperative visuospatial attention measures, including the Posner cueing task. Our primary outcome was maximum POD severity, measured by the Confusion Assessment Method Severity (CAM-S) short form. Secondary outcomes included falls, hospital readmission, and Zarit caregiver burden rating, measured three-months post-surgery. Data were summarized (i.e., frequencies, mean (SD), and median [Q1, Q3]) and analyzed (i.e., Spearman correlational testing). RESULTS: The majority of the 45 participants were female (58%) and white (93%), with mean (SD) age 74.2 (5.4) years and 15.6 (2.7) years of education. 69% were not delirious post-surgery, 18% were classified as subsyndromal (CAM-S > 1), and 13% had POD. The delirium score's median [Q1, Q3] value was 0 [0, 2.0]. The median [Q1, Q3] value for stimulus reaction time was 510 ms [463,558]. The correlation coefficient (p-value) between delirium and Posner stimulus reaction time was 0.45 (p < 0.001). Correlation coefficients were in the expected direction but not significant between Posner stimulus reaction time and three-month outcomes. Delirium severity was correlated with caregiver burden (0.34, p = 0.044). CONCLUSION: Data continues to demonstrate that preoperative measures of visual attention predict POD. Additionally, POD measured in this study predicts caregiver burden at three months, supporting the importance of this finding. Further studies with more participants can help to determine how to apply measures of visual attention to better predict and monitor the effects of delirium on cognition and neurodegeneration. Understanding this relationship provides a basis for future research on strategies to prevent, mitigate, or rehabilitate the effects of delirium, improving hospital outcomes and potentially delaying or preventing dementia. Funding AACSF-22-928731; K07AG066813.

  PublisherOA PDFDOI

• Informing etiological heterogeneity of mild cognitive impairment and risk for progression to dementia with plasma p-tau217

  The Journal of Prevention of Alzheimer s Disease · 2025-01-01 · 9 citations

  articleOpen access

  Mild cognitive impairment (MCI) is a clinical diagnosis representing early symptom changes with preserved functional independence. There are multiple potential etiologies of MCI. While often presumed to be related to Alzheimer's disease (AD), other neurodegenerative and non-neurodegenerative causes are common. Wider availability of relatively non-invasive plasma AD biomarkers, such as p-tau217, can provide invaluable insights into MCI clinico-pathology and the associated implications for symptom etiology, prognosis (e.g., risk for progression to dementia), and treatment options. The main goal of this study was to evaluate differences between individuals with MCI with and without plasma p-tau217 biomarker evidence of AD (MCI AD+ and MCI AD- ) as well as a control group of clinically normal older adults with negative AD biomarkers (CN AD- ). We evaluated group differences in demographics, recruitment, clinical scales, fluid biomarkers, and brain imaging. We further probed these factors as independent contributors to symptoms among MCI AD- participants, for whom symptom etiology is most poorly understood. Lastly, in a subset of participants followed longitudinally, we investigated how these factors related to odds of clinical progression to dementia. We conducted an observational cross-sectional and longitudinal clinical research study. Study groups were compared cross-sectionally on demographics, recruitment, clinical measures, and biomarkers (chi square analyses, analyses of covariance). Contributors to functional changes were evaluated with multiple linear regression. Factors associated with the odds of progression from MCI to dementia longitudinally were evaluated with binary logistic regression. 1Florida Alzheimer's Disease Research Center. Cross-sectional analyses included 378 older adults classified as CN AD- ( N = 76, age 66.1 ± 7.2, 63.2% female, 23.7% non-Hispanic/White), MCI AD- ( N = 198, age 68.9 ± 7.9, 51.5% female, 29.3% non-Hispanic/White), or MCI AD+ ( N = 104, age 73.9 ± 7.4, 52.9% female, 49.0% non-Hispanic/White). Longitudinal analyses focused on 207 participants with MCI (68.5% of cross-sectional MCI sample) followed for an average of 3 years. Demographics (age, sex, years of education, self-identified race and ethnicity, primary spoken language), National Alzheimer's Coordinating Center-defined clinical phenotypes (Clinically Normal, Impaired – Not MCI, Amnestic MCI, Nonamnestic MCI, Dementia), recruitment source (clinic-based versus community-based), genetics ( APOE genotype), functional evaluation (Clinical Dementia Rating scale), global cognition (Mini Mental State Exam), vascular history (Vascular Burden Score), neuropsychiatric symptoms (NPI-Q Total score), plasma biomarkers (ALZPath p-tau217, Quanterix Simoa-based GFAP and NfL), and brain imaging (grey matter volume in select AD-relevant regions of interest, global white matter hyperintensity volume). Among those with MCI, 104 (34.4%) had plasma biomarker evidence of AD. MCI AD+ participants were more frequently recruited from clinic-based settings than MCI AD- (74.8% vs. 47.5%, p <.001). Over half (51.5%) of MCI AD+ carried at least one APOE e4 allele compared to 26.6% of MCI AD- and 29.4% of CN AD- ( p <.001). Both MCI AD+ ( p <.001, Cohen's d = 0.93) and MCI AD- ( p <.001, d = 0.75) reported more severe neuropsychiatric symptoms than CN AD. MCI AD+ had higher plasma GFAP and NfL than both MCI AD- (GFAP: p <.001, d = 0.88, NfL: p <.001, d = 0.86) and CN AD- (GFAP: p <.001, d = 0.80; NfL: p <.001, d = 0.89). For the AD signature region of interest, MCI AD+ had lower volume than both CN AD- ( p <.001, d = 0.78) and MCI AD- ( p =.018, d = 0.39). For the hippocampus, both MCI AD+ ( p <.001, d = 0.87) and MCI AD- ( p <.001, d = 0.64) had lower volume than CN AD- . Longitudinally, older age (OR=1.14 [1.06–1.22], p <.001), higher levels of p-tau217 (OR=10.37 [3.00–35.02], p <.001) and higher neuropsychiatric symptoms (OR=1.19 [1.02–1.39], p =.023) were associated with higher odds of progression to dementia. MCI is etiologically heterogeneous. The presence of Alzheimer's pathology defined by elevated plasma p-tau217 in individuals with MCI significantly worsens prognosis. Neuropsychiatric symptoms may contribute to cognitive complaints and risk for progressive decline irrespective of AD pathology. Plasma p-tau217 can inform our understanding of base rates of different MCI phenotypes on a larger scale. As with other AD biomarkers, frequency of elevated plasma p-tau217 and odds of progression to dementia requires careful consideration of recruitment source (clinic- vs. community-based), especially across ethno-racially diverse older adults. Ongoing integration of emerging neurodegenerative disease biomarkers with detailed clinical evaluations will continue to improve treatment specificity and prognosis.

  PublisherDOI

• Impact of Worry on Experimental Hippocampal Tasks and Hippocampal Volumetrics in Older Adults with Subjective Cognitive Complaints

  Alzheimer s & Dementia · 2025-12-01

  articleOpen access

  BACKGROUND: Subjective cognitive complaints (SCC) have been associated with decreased hippocampal volume and those with distress about their SCC have a higher risk of preclinical Alzheimer's disease (AD). The current study divided individuals with SCC into "worried" and "non-worried" groups to determine whether 1) experimental hippocampal tasks and hippocampal volumetrics differ between groups and 2) determine if mood and/or motivation were driving differences. METHOD: Participants were 154 adults (mean age = 71±5 years, mean education = 16±2 years, 62% female, 87% white) with SCC. There were two groups: "worried" (N = 76) or "non-worried" (N = 78) about cognitive changes over the past five years (Cognitive Change Index). Cognitive (two hippocampal-based experimental tasks: ARENA (spatial navigation) and the Mnemonic Similarity Task (MST; pattern separation)), mood (Beck Depression Inventory-II (BDI-II), Apathy Scale (AS), and the State-Trait Anxiety Inventory (STAI)), and neuroimaging data were drawn from the baseline visit. Hippocampal imaging was performed using high-resolution T2 sequences (0.39x0.39mm). Whole hippocampal and CA1, CA3, and dentate gyrus volumetrics were analyzed with Freesurfer version 7.1.1. based on proposed neural correlates of ARENA and MST. Data were analyzed with independent t-tests and ANCOVAs, with demographic and mood/motivation as covariates. RESULTS: The worried group performed significantly worse on ARENA learning (t(152)=-2.7, p = 0.004), recall (t(152)=-2.2, p = 0.02), and overall composite memory z-scores (t(152)=3.3, p < 0.001). There were no significant differences observed on the MST or hippocampal volumetrics between groups. The worried group reported greater depression (t(152)=-2.4, p = 0.01), trait anxiety (t(152)=-2.6, p = 0.01), apathy (t(152)=-2.2, p = 0.01) on self-report measures. ANCOVAs revealed that apathy significantly contributed to ARENA performance on learning (F(1,152)=6.7, p = 0.01) and recall composites (F(1,152)=5.4, p = 0.02), reducing group difference on learning composite only. Overall memory composite remained significant without demographic or mood contributions (F(1,152)=6.9, p = 0.009). CONCLUSIONS: Older adults with SCC worry exhibit higher levels of mood and motivation symptoms, which may contribute to poorer performance on cognitive tasks. Two hypotheses are possible: 1) greater mood symptoms are driving SCC and ARENA performance, or 2) ARENA may be uniquely sensitive to detect memory changes, as its neural correlates are implicated in early AD. Since mood symptoms are common in preclinical AD, the worried SCC group may reflect this preclinical change.

  PublisherOA PDFDOI

• Continuous Glucose Monitoring in Insulin-Treated Older Adults With Diabetes and Alzheimer Disease and Related Dementias

  JAMA Network Open · 2025-12-02 · 1 citations

  articleOpen access

  Importance: Cognitive impairment and glycemic control have a bidirectional association. Understanding the impact of continuous glucose monitoring (CGM) vs self-monitoring of blood glucose (SMBG) is important for treating older adults with Alzheimer disease and related dementias (ADRD) and diabetes that is treated with insulin. Objective: To compare the risks of glycemic outcomes and related adverse events between CGM users and prevalent SMBG users in insulin-treated older adults with ADRD and diabetes. Design, Setting, and Participants: This retrospective, prevalent-new user cohort study utilized a nationwide, 15% random sample of Medicare claims data (Parts A, B, and D) from January 2016 to December 2020 to ensure balanced cohorts. Insulin-treated older adults (≥66 years) with ADRD and diabetes were included. Individuals in hospice care or with a professional CGM use were excluded. Analysis was carried out from August 2023 to December 2024. Exposure: Therapeutic CGM use vs prevalent SMBG use. Main Outcomes and Measures: Primary outcomes included hypoglycemia hospitalizations, hyperglycemia crisis, and all-cause mortality; falls and all-cause hospitalizations were secondary outcomes. Upper respiratory tract infections served as a negative control outcome. A 1:1 propensity score matching with a 0.25 caliper was carried out for confounding control. Cox proportional hazards models were used for outcome analysis. Results: In this cohort of 2022 insulin-treated older adults with diabetes and ADRD (1011 CGM users and 1011 SMBG users; mean [SD] age, 76.4 [6.7] years; 1133 female [56.0%]), CGM use was significantly associated with lower risk of all-cause hospitalization (hazard ratio [HR], 0.86; 95% CI, 0.76-0.96) and mortality (HR, 0.57; 95% CI, 0.48-0.67) compared with SMBG use. CGM use had lower point estimates for hypoglycemia hospitalization (HR, 0.66; 95% CI, 0.40-1.08) and falls (HR, 0.86; 95% CI, 0.68-1.08) and higher point estimates for hyperglycemia crisis (HR, 1.38; 95% CI, 0.99-1.94) vs SMBG use, but these findings were not significant. Exploratory subgroup analyses showed varied benefits. The negative control outcome showed no significant differences across analyses. Conclusions and Relevance: In this cohort study of insulin-treated older adults with ADRD and diabetes, CGM use was associated with improved long-term clinical outcomes. Pragmatic (ie, evaluating the effectiveness of healthcare interventions in everyday settings) trials are needed to validate these findings and to assess the feasibility of CGM use in this population.

  PublisherOA PDFDOI

• Moderating effects of plasma glial fibrillary acidic protein along the Alzheimer's disease continuum

  Alzheimer s & Dementia · 2025-09-01 · 2 citations

  articleOpen access

  Abstract INTRODUCTION Glial fibrillary acidic protein (GFAP) may contribute to Alzheimer's pathology at early disease stages. GFAP moderation of Alzheimer's disease (AD)‐related neurodegeneration and cognition is unclear. METHODS We examined plasma GFAP moderation of AD biomarkers (amyloid beta [Aβ]‐positron emission tomography [PET][A]; plasma phosphorylated tau‐181 [p‐tau181][T 1 ]), neurodegeneration (plasma NfL[N plasma ]; structural magnetic resonance imaging [MRI][N MRI ]), and cognition (Cog memory ; Cog executive ) in two cohorts: University of California San Francisco (UCSF) ( N = 212, 91.0% non‐Hispanic/Latino White [NHLW], age = 74.7 [7.6] years, 75.9% cognitively unimpaired [CU]) and 1Florida Alzheimer's Disease Research Centers (1FLADRC; N = 582, 32.8% NHLW, age = 70.7 [8.5] years, 28.9% CU). RESULTS Plasma GFAP consistently moderated A–T 1 (UCSF: β = 0.46, p = 0.012; 1FLADRC: β = 0.12, p = 0.029). The association between elevated Aβ‐PET and increased (p‐tau) was strengthened at higher GFAP concentrations. In 1FLADRC, GFAP moderated T 1 –N plasma/MRI. In UCSF, GFAP moderated T 1 –Cog memory/executive and N MRI –Cog memory/executive . Higher GFAP consistently related to worse neurodegeneration and cognition (main effects). DISCUSSION Across demographically and clinically heterogeneous cohorts, plasma GFAP is a key moderator of AD and may help identify individuals at greatest risk of AD‐related neurodegeneration and cognitive decline. Highlights AD biomarkers were measured in two demographically and clinically distinct cohorts. Plasma GFAP moderated Aβ‐PET to p‐tau associations in both UCSF and 1FLADRC. Cohort‐dependent, GFAP moderated p‐tau to neurodegeneration and cognition associations. All moderations revealed strengthened disease associations with higher plasma GFAP. Plasma GFAP may help identify individuals at greatest risk of AD‐related decline.

  PublisherOA PDFDOI

• Risk of Seizure Associated With Concomitant Use of Tramadol and Antidepressants in Older Nursing Home Residents

  Neurology · 2025-10-08

  articleOpen access

  BACKGROUND AND OBJECTIVES: Concomitant use of tramadol and antidepressants with potent inhibition of the cytochrome P450 2D6 (CYP2D6) enzyme is postulated to increase risk of seizures in older adults; yet, such an association has not been empirically tested in populations. We aimed to examine the association of concomitant tramadol and CYP2D6-inhibiting vs CYP2D6-neutral antidepressant use and the risk of seizures among older nursing home (NH) residents. METHODS: This population-based cohort study was conducted using a 100% Medicare NH sample from January 2010 to December 2021. We included long-term residents aged 65 years or older who initiated antidepressants on existing tramadol use (tramadol-antidepressant users) or initiated tramadol on existing antidepressant use (antidepressant-tramadol users). Patients were followed up until the end of 1 year, NH discharge, death, or study end. The key exposure was concomitant use of tramadol with CYP2D6-inhibiting vs CYP2D6-neutral antidepressants. The key outcome was incident rates of medical encounters with a diagnosis of seizure and analyzed using negative binomial or Poisson regression models adjusted for baseline covariates (e.g., pain status and depressive, physical, and cognitive function) through the inverse probability of treatment weighting. RESULTS: We identified 11,162 concomitant tramadol-antidepressant users (mean [SD] age, 86.2 [8.5] years; 9,077 [81.3%] female) and 58,994 concomitant antidepressant-tramadol users (mean [SD] age, 85.3 [8.4] years; 47,053 [79.8%] female). The incidence rate of seizures was 16.10 and 20.17 per 100 patient-years, respectively, for the tramadol-antidepressant and antidepressant-tramadol group. In both subgroups, co-use of tramadol with CYP2D6-inhibiting (vs with CYP2D6-neutral) antidepressants was associated with higher adjusted incidence rate ratios of seizures (1.09 [95% CI 1.02-1.18] and 1.06 [95% CI 1.03-1.10]). Findings were corroborated by a negative control exposure analysis in which co-use of hydrocodone with CYPD2D6-inhibiting (vs CYP2D6-neutral) antidepressants was not associated with risk of seizures. DISCUSSION: Concomitant use of tramadol with CYP2D6-inhibiting vs CYP2D6-neutral antidepressants was associated with increased risk of seizures. Findings are only generalizable to long-term NH populations and are subject to residual confounding. Clinicians should be mindful of seizure risk in older patients who use tramadol concomitantly with antidepressants, particularly CYP2D6-inhibiting antidepressants. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that the combination of tramadol and CYP2D6-inhibiting antidepressants is associated with a higher risk of seizures compared with the combination of tramadol and CYP2D6-neutral antidepressants.

  PublisherOA PDFDOI

• Semantic intrusion errors differentiate between amnestic MCI who are plasma p-tau217+ from p-tau217- after adjusting for initial learning strength

  Frontiers in Neurology · 2025-07-22 · 2 citations

  articleOpen access

  Background Semantic intrusion errors (SIEs) are associated with mild cognitive impairment (MCI) due to Alzheimer's disease (AD). It is unknown whether accounting for maximum learning capacity still leads to an increase in SIEs when elevated plasma p-tau 217 , a biological indicator of underlying AD, is present. Methods One hundred fifty-eight older adult participants completed the Loewenstein-Acevedo Scales for Semantic Interference and Learning (LASSI-L), a sensitive cognitive challenge test designed to elicit SIEs. Of these, 108 were clinically diagnosed with amnestic MCI (aMCI). Fifty-eight individuals met or exceeded a plasma p-tau 217 positivity of &amp;gt; 0.5 5 pg/ml, while 50 individuals scored below this threshold. Results After adjusting for demographic covariates and maximum learning capacity, the aMCI p-tau 217 + group evidenced more SIEs compared to aMCI p-tau 217 - on the first (list B1; p = 0.035) and second trials of the competing list (list B2; p = 0.006). Biological predictors such as ApoE ε4 status, higher p-tau 217 , and older age were predictors of an elevated number of SIEs [list B2: F (3,104) = 10.92; p = 0.001; R = 0.489)]. Conclusions Unlike previous studies that used amyloid PET or other plasma biomarkers, individuals with aMCI p-tau 217 + evidenced more SIEs, even after adjusting for their initial learning capacity, a covariate that has not been studied previously. These findings support that SIEs are more prevalent in the presence of underlying AD pathology and occur independent of learning deficits.

  PublisherOA PDFDOI

• Sex‐stratified genome‐wide meta‐analysis identifies novel loci for cognitive decline in older adults

  Alzheimer s & Dementia · 2025-03-01 · 2 citations

  reviewOpen access

  Abstract INTRODUCTION Many complex traits and diseases show sex‐specific biases in clinical presentation and prevalence. METHODS To understand sex‐specific genetic architecture of cognitive decline across five cognitive domains (attention, memory, executive function, language, and visuospatial function) and global cognitive function, we performed sex‐stratified genome‐wide meta‐analysis in 3021 older adults aged ≥ 65 years (female = 1545, male = 1476) from three prospective cohorts. Gene‐based and gene‐set enrichment analyses were conducted for each cognitive trait. RESULTS We identified a novel genome‐wide significant (GWS) intergenic locus for decline of memory in males near RPS23P3 on chromosome 4 (rs6851574: minor allele frequency [MAF] = 0.39, P male = 4.10E‐08, β male = 0.19; P interaction = 3.76E‐04). We also identified a subthreshold GWS locus for decline of executive function on chromosome 12 in females near the NDUFA12 gene, involved in oxidative phosphorylation (rs11107823: MAF = 0.12, P female = 9.35E‐08, β female = 0.28; P interaction = 7.42E‐06). DISCUSSION Sex‐aware genetic studies can help in the identification of novel genetic loci and enhance sex‐specific understanding of cognitive decline. Highlights Our genome‐wide meta‐analysis of single variants identified two new genetic associations, one in males and one in females. The novel male association was observed with the decline of memory in the intergenic region near the RPS23P3 gene on chromosome 4. This intergenic region has previously been implicated in several brain and cognition related traits, including anatomical brain aging, brain shape, and educational attainment. The novel female‐specific association was observed with decline in executive function on chromosome 12 near the NDUFA12 gene, which is involved in oxidative phosphorylation. Sex‐stratified analyses offer sex‐specific understanding of biological pathways involved in cognitive aging.

  PublisherOA PDFDOI

• Prescription opioid use and cognitive function in older adults with chronic pain: A population‐based longitudinal cohort study

  Alzheimer s & Dementia · 2025-02-01 · 2 citations

  articleOpen accessSenior author

  INTRODUCTION: Whether prescription opioid exposure, duration, and dose are associated with cognitive function remains inconclusive. METHODS: A longitudinal cohort among 3097 older adults with chronic pain and without dementia was conducted using Health and Retirement Study (HRS) linked to Medicare data from 2006 to 2020. Prescription opioid exposure, cumulative use for ≥ 90 days, and high-dose use (≥ 90 morphine milligram equivalents [MME] daily) were assessed biennially. Memory score and dementia probability were derived from HRS cognitive measures and analyzed using linear mixed-effects models. RESULTS: Adjusted memory decline and dementia probability were not statistically different between patients with (vs. without) opioid exposure and between patients with cumulative use for ≥ 90 days (vs. < 90 days) but were higher between participants with high-dose opioid use (vs. low-dose) at the end of the follow-up. DISCUSSION: Prescription opioid exposure and duration were not associated, but high-dose opioid use was associated with greater memory decline and dementia probability. HIGHLIGHTS: Opioid use versus no use was not related to memory decline and dementia probability. Long-term opioid use was not related to memory decline and dementia probability. High-dose opioid use was related to greater memory decline and dementia probability.

  PublisherOA PDFDOI

Recent grants

• NIH Grant U01AT000162

  NIH · $37.7M · 2011

• Project 4 (Pitts)-Cholinergic and amyloid alteration in mild cognitive impairment

  NIH · $67.4M · 1997–2027

• NIH Grant P01NS030318

  NIH · $7.3M · 2012

• NIH Grant P30MH049815

  NIH · $1.8M · 1998

• The role of astrogliosis in aging and the pathological and clinical progression of Alzheimer's Disease

  NIH · $98.8M · 2004–2028

Frequent coauthors

• Oscar L. López

  University of Pittsburgh

  339 shared

• William E. Klunk

  268 shared

• Chester A. Mathis

  University of Pittsburgh

  217 shared

• James T. Becker

  First Solar (United States)

  176 shared

• Ranjan Duara

  Florida College

  166 shared

• M. Ilyas Kamboh

  University of Pittsburgh

  159 shared

• Lewis H. Kuller

  University of Pittsburgh

  156 shared

• Julie C. Price

  Massachusetts General Hospital

  146 shared

Labs

• iBRAIN LabPI

Education

• M.D.

  University of Florida

  1974

• Other, Neurology

  University of Florida

• Other, Neurochemistry

  University of Virginia Center for Neurosciences

• Other, Psychology and Neuroscience

  University of Florida

Awards & honors

• Best Doctors in America 2003-2013