Neuroimaging PheWAS and molecular phenotyping implicate PSMC3 in Alzheimer’s disease.
Bledsoe X, Wang TC, Wu Y, Archer D, Chen HH, Naj AC, Bush WS, Hohman TJ, Dumitrescu L, Below JE, Gamazon ER.
Alzheimers Dement. 2026 Feb;22(2):e71217. doi: 10.1002/alz.71217.
PMID: 41732108 Free PMC article.
Abstract
Introduction: Neuroimaging genetics has advanced our understanding of Alzheimer’s disease (AD); however, frameworks using functional genomics are needed to elucidate mechanisms connecting loci to neurological outcomes. To address this need, we explored relationships between AD-associated variants and disease via their impact on gene expression and neuroanatomical phenotypes.
Methods: We mapped established AD genes to neuroimaging traits using the NeuroimaGene Atlas and predicted transcript-driven neurological features of AD by comparing gene-derived neuroimaging features with clinical neuroimaging data. Genetic covariance analyses were performed to characterize shared genetic architecture between AD endophenotypes and neuroimaging features, and to identify neuroimaging features associated with a family history of dementia.
Results: Our analyses implicate PSMC3 as a contributor to AD pathophysiology and identify AD endophenotypes, including dementia family history, linked to frontal cortex thickness and volume, as well as changes in cerebrospinal fluid volume.
Discussion: Our findings prioritize AD genes whose regulation is associated with vulnerable brain regions, offering a potential mechanistic framework for downstream functional validation.
Keywords: Alzheimer’s disease; NeuroimaGene; dementia family history; genetic covariance; neuroimaging‐derived phenotypes; transcriptome‐wide association studies.
How much of a face is a face: exploring reidentification potential with generative AI.
Cho C, Liu Y, Jiang B, McNeil AJ, Dawant BM, Landman BA, Tkaczyk ER.
J Med Imaging (Bellingham). 2026 Feb;13(Suppl 1):S11202. doi: 10.1117/1.JMI.13.S1.S11202. Epub 2026 Feb 15.
PMID: 41700218 Free PMC article.
Abstract
Purpose: Clinical photographs play an integral role across medical fields. Since the mid-20th century, deidentification has consisted of black bars covering specific facial features, typically the eyes alone. Although increasingly questioned, this practice persists in clinical and academic settings.
Approach: A barrier to standardized deidentification guideline development is the unknown risk of artificial intelligence (AI) to reconstruct faces from partially obscured photos. We evaluate the ability of generative AI to reconstruct 10,000 facial images in the Synthetic Faces High Quality dataset across 14 regional masking strategies.
Results: Covering the eyes or any other single facial feature resulted in highly identifiable reconstructions, demonstrated by low face mesh distortion (0.14 to 0.18 relative to whole-face masking; absolute total face mesh distortion 8.34 to 10.19) and high structural similarity index to the original face (1.24 to 1.25 relative to whole-face masking; absolute SSIM 0.91 to 0.92). An open-source face verification model using Dlib was able to match 97.98% to 99.93% of these reconstructed images with the original image prior to single feature masking. Removing all major facial features (eyebrows, eyes, nose, and mouth) resulted in a threefold reduction in face verification rates compared with eyes alone, from 98.87% (95% CI [98.63%, 99.07%]) to 33.93% (95% CI [32.95%, 34.94%]).
Conclusions: We provide quantitative metrics of the reidentification risk that modern generative AI technology poses for partially obscured facial images.
Keywords: deidentification; facial images; generative AI; latent diffusion model; privacy; reidentification.
Single cell protein profiling of focal cortical dysplasia in a patient requiring multiple resections.
Elsayed NA, Naftel RP, Mobley BC, Alexander AL, Toland AM, Brockman AA, Irish JM, Ihrie RA, Ess KC.
Acta Neuropathol Commun. 2026 Mar 13. doi: 10.1186/s40478-026-02273-3. Online ahead of print.
PMID: 41827061 Free article. No abstract available.
No abstract available
Keywords: AKT3; Epilepsy; Focal cortical dysplasia; Gain of function; Mass cytometry.
A Community–Informed Toolkit for Physician-Scientist Competencies and Milestones: Bridging the Worlds of Medicine and Research.
Estrada L, Baca JT, Baron MH, Brass LF, Craft CS, Cavazos JE, Kao AW, Roghmann MC, Yellin J, McCormack WT.
Acad Med. 2026 Feb 28:wvag053. doi: 10.1093/acamed/wvag053. Online ahead of print.
PMID: 41766344
Pathway to Adaptive Neuromodulation: Modeling Epileptogenic Brain States Using SEEG.
Makhoul GS, Johnson GW, Reda A, Hidalgo Monroy Lerma B, Fan JM, Worrell GA, Englot DJ.
Epilepsy Curr. 2026 Feb 19:15357597261422447. doi: 10.1177/15357597261422447. Online ahead of print.
PMID: 41726571 Free PMC article.
Abstract
Neuromodulation is becoming a common treatment strategy for patients with drug-resistant epilepsy who are not candidates for resective surgery. Responsive neurostimulation can effectively reduce seizure burden, however it remains unclear which neural signals are most important for triggered stimulation. Furthermore, the high-dimensional parameter space remains systematically underexamined. As more patients become candidates for neurostimulation, clinical teams will need to decide on the optimal site and stimulation program for therapeutic neuromodulation. In this review, we highlight how recent insight into the biological rhythms of epilepsy may pair with personalization protocols in the emerging field of neuropsychiatric neuromodulation. Finally, we discuss future directions for epilepsy neuromodulation, specifically how machine learning can offer clinical teams actionable feedback on neuromodulation efficacy.
Keywords: clinical translation; electrophysiology; epilepsy; machine learning; neuromodulation
Clonal Hematopoiesis and Risk of Incident Pericarditis and Myocarditis in 2 US Biobank Cohorts.
Pershad Y, Zhao K, Heimlich JB, Bick AG.
JAMA Cardiol. 2026 Mar 18:e260258. doi: 10.1001/jamacardio.2026.0258. Online ahead of print.
PMID: 41848713 Free PMC article.
No abstract available
Trained immunity: new paradigm in the immunological memory of cardiovascular disease.
Hope E, Gonzalez AL, Norman LS, Smith HC, Wassenaar JW, Vickers KC, Brown JD, Doran AC.
Immunohorizons. 2026 Feb 17;10(SI):vlag008. doi: 10.1093/immhor/vlag008.
PMID: 41723637 Free PMC article. Review.
Abstract
Cardiovascular disease (CVD) remains the leading cause of death worldwide, despite significant progress in identifying and managing traditional risk factors such as hyperlipidemia, hypertension, and diabetes. While targeted therapies addressing these factors reduce the risk of primary and secondary cardiac events, a substantial “residual risk” persists even after successful clinical intervention. This residual risk has prompted renewed interest in understanding the long-term biological effects of cardiovascular risk factors, particularly through the lens of chronic inflammation. Recent advances highlight a pivotal role for trained immunity-a form of innate immune memory driven by epigenetic and metabolic reprogramming-in driving this inflammation. Unlike adaptive immune memory, trained immunity occurs in innate immune cells and enhances their responsiveness to subsequent, unrelated stimuli. Emerging evidence suggests that various cardiovascular risk states, including hypercholesterolemia, obesity, and diabetes, can induce trained immunity, leading to heightened inflammatory tone that persists over time. Cardiac macrophages, as central mediators of tissue homeostasis and inflammation in the heart, are increasingly recognized as critical targets of this phenomenon. In this review, we explore how established cardiovascular risk factors can induce trained immunity on cardiac macrophages and examine the implications for disease progression, myocardial remodeling, and post-injury repair. Finally, we discuss emerging therapeutic strategies aimed at modulating trained immunity to reduce residual cardiovascular risk, offering a new frontier in the prevention and treatment of CVD.
Keywords: inflammation; memory; monocyte/macrophages.
Human cranial stem cells: developmental, pathologic, and therapeutic implications.
Reddy A, Means A, Qaddo S, Tong V, Gergoudis F, Alter N, Torres-Guzman R, Golinko M, Thayer W, Galdyn I, Perdikis G, Pontell ME.
Front Cell Dev Biol. 2026 Feb 12;14:1718526. doi: 10.3389/fcell.2026.1718526. eCollection 2026.
PMID: 41768990 Free PMC article. Review.
Abstract
Cranial skeletal stem cells are central to skull development, maintenance, and repair. These stem cell populations balance self-renewal with lineage commitment, providing osteogenic, chondrogenic, and stromal outputs required for craniofacial growth. While bone grafting remains the gold standard for reconstruction, limitations in donor supply and morbidity have driven interest in harnessing endogenous regenerative programs. In this review, we synthesize current knowledge of human cranial stem cell biology, drawing on developmental, molecular, and imaging data. We delineate their distinct niches within the sutures, dura, and periosteum, as well as the signaling pathways that regulate their function. We then highlight future avenues of investigation, including high-resolution profiling of human stem cell populations and development of mechanism-based regenerative strategies that integrate cell therapy with scaffold design.
Keywords: cranial development; craniofacial regeneration; craniosynostosis; regenerative therapeutics; skeletal stem cells; stem cell signaling; tissue engineering.
Targeting β-catenin: PROTACs and precision degraders for Wnt-driven cancers.
Trapani J, Caroland KP, Ahmed Y, Robbins DJ, Weiss VL, Lee E.
Front Oncol. 2026 Feb 2;16:1777843. doi: 10.3389/fonc.2026.1777843. eCollection 2026.
PMID: 41704615 Free PMC article. Review.
Abstract
The Wnt signaling pathway, a highly conserved molecular cascade, orchestrates critical biological processes including embryonic development, cell differentiation, and proliferation across diverse organisms. Despite the pivotal role that Wnt signaling plays in many diseases, most notably cancer, there are still no FDA-approved, efficacious drugs available that inhibit this pathway. Most Wnt inhibitors target upstream components (e.g., Wnt ligand production and receptors) rather than the most commonly mutated downstream proteins in the pathway. Consequently, there is considerable interest in developing drugs that target the downstream effector, β-catenin. This review examines the challenges in targeting β-catenin, current approaches, and insights into overcoming on-target toxicity associated with cadherin-bound β-catenin.
Keywords: PROTAC (proteolysis targeting chimera); Wnt; beta-catenin; drug discovery; toxicity.
Leveling the Playing Field in Vestibular Schwannoma Outcome Reporting: A Survey of Variance and Bias in Published Research.
Marinelli JP, Gauhar F, Grisham CJ, Dambrino Iv RJ, Kelly PD, Carlson ML.
Otol Neurotol. 2026 Mar 10. doi: 10.1097/MAO.0000000000004886. Online ahead of print.
PMID: 41803056
Impact of CYP2D6 Metabolizer Status on Ondansetron Efficacy in Early Pregnancy Induced Nausea and Vomiting: A Case Control Study.
Liu M, Shuey MM, Holley SE, Fountain DF, Jaworski J, Griffin C, Kim J, Stec M, Sunthankar SD, Ong HH, Gangireddy S, Wei WQ, Gaedigk A, Velez Edwards DR, Kawai VK.
Clin Transl Sci. 2026 Mar;19(3):e70523. doi: 10.1111/cts.70523.
PMID: 41820792
Impact of using PRS-CSx and pruning and thresholding for polygenic partitioning of apparent treatment resistant hypertension.
Seagle HM, Kim J, Akerele AT; VA Million Veteran Program; Hung A, Hellwege JN, Edwards TL.
Pac Symp Biocomput. 2026;31:664-678. doi: 10.1142/9789819824755_0048.
PMID: 41758176 Free article.
Software Application Profile: McBias: a user-friendly R package and RShiny application for modeling bias in observational studies.
Breidenbach A, Blostein F, Petty A, Lake AM, Aldrich M, Gamazon ER, Tao R, Below J, Khankari NK.
Int J Epidemiol. 2026 Feb 18;55(2):dyag004. doi: 10.1093/ije/dyag004.
PMID: 41747259 No abstract available.
Mucosal vaccination clears Clostridioides difficile colonization.
Thomas AK, Peritore-Galve FC, Ehni AG, Lança BBC, Coggin J, Brady EJ, Yoder SM, Shrem R, Rodríguez RC, Kroh HK, Gibson-Corley KN, Kay Washington M, Olivares-Villagómez D, Creech CB, Nicholson MR, Spiller BW, Lacy DB.
Nature. 2026 Feb 18. doi: 10.1038/s41586-026-10138-x. Online ahead of print.
PMID: 41708852
Ovarian hormones and obesity drive Th17-mediated airway inflammation through estrogen receptor-α signaling.
Henriquez Pilier E, Cephus JY, Kuehnle SN, Tannous E, Tomasello A, McKernan KE, Peebles RS Jr,, Cahill KN, Rathmell JC, Newcomb DC.
Am J Physiol Lung Cell Mol Physiol. 2026 Apr 1;330(4):L267-L273. doi: 10.1152/ajplung.00400.2025. Epub 2026 Feb 13.
PMID: 41686163 Free article.
Clinical Note-Extracted Psychosocial Factors for Predicting Suicide Attempt Among ED Patients With Suicidal Ideation.
Lee H, Jadhav K, Ripperger M, Coleman PL, Morley TJ, Palmer SA, Han L, Chen Q, Bejan CA, Ruderfer DM, Walsh CG.
JAMA Netw Open. 2026 Mar 2;9(3):e260589. doi: 10.1001/jamanetworkopen.2026.0589.
PMID: 41779393 Free PMC article.
Stacking sternotomies: Does surgical history predict post-transplant risk?
Navid W, Wang CC, Chawla E, Kayali Z, Eidson C, Ahmad A, Petrovic M, Trahanas J, Bommareddi S, Williams AM, Quintana E, Absi T, Bacchetta M, Shah AS, Lima B.
JHLT Open. 2026 Feb 16;12:100523. doi: 10.1016/j.jhlto.2026.100523. eCollection 2026 May.
PMID: 41846602 Free PMC article.
Association of Clonal Hematopoiesis with Incident, Late-Onset, Seropositive Rheumatoid Arthritis.
Zhao K, Pershad Y, Heimlich JB, Ormseth M, Stein CM, Sharber B, Vlasschaert C, Bick AG, Corty RW.
Arthritis Rheumatol. 2026 Mar 18. doi: 10.1002/art.70133. Online ahead of print.
PMID: 41847932
Improved Outcomes and Donor Utilization in Heart Transplantation with 10°C static cold storage.
Ahmad A, Williams AM, Bommareddi S, Lima B, Absi T, Quintana E, Wang CC, Petrovic M, McGann K, Devries S, Lowman J, Siddiqi H, Amancherla K, Menachem JN, Rali AS, Scholl SR, Schwartz CA, Keck C, Bacchetta M, Schlendorf K, Shah AS, Trahanas JM.
J Heart Lung Transplant. 2026 Feb 23:S1053-2498(26)00058-6. doi: 10.1016/j.healun.2026.02.004. Online ahead of print.
PMID: 41740940
Oxygen Extraction Trajectories During Cardiopulmonary Bypass Impact Postoperative Outcomes in Coronary Artery Bypass Grafting.
Ahmad A, Williams AM, Trahanas J, Bommareddi S, Wang CC, Petrovic M, Absi T, Quintana E, Lombard FW, Billings FT 4th, McIlroy D, Bacchetta M, Shah AS, Lima B.
J Thorac Cardiovasc Surg. 2026 Feb 26:S0022-5223(26)00175-3. doi: 10.1016/j.jtcvs.2026.02.018. Online ahead of print.
PMID: 41763386 Free article.
Double whammy: increased severe primary graft dysfunction after prolonged warm ischemia and inadequate oxygen delivery during heart transplant.
Wang CC, Ahmad A, Petrovic M, Navid W, Eidson C, Trahanas J, Williams AM, Bommareddi S, Nguyen DQ, Absi T, Quintana E, DeVries S, Lepore JA, Warhoover M, Rali AS, Schlendorf KH, Bacchetta M, Shah AS, Lima B.
Front Transplant. 2026 Feb 24;5:1737467. doi: 10.3389/frtra.2026.1737467. eCollection 2026.
PMID: 41816020 Free PMC article.
The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.
Nicholson MR, Ma S, Strickland BA, Cecala M, Zhang L, Reasoner S, Guiberson ER, Munneke MJ, Shilts MH, Skaar EP, Das SR.
J Infect Dis. 2026 Mar 17;233(3):e812-e822. doi: 10.1093/infdis/jiaf631.
PMID: 41379981 Free PMC article.
Estradiol treatment induces both shared and unique gene regulation and networks in adipose cell types of gonadectomized obese XX and XY mice.
Zhao Y, Liu R, Ng JP, Yu S, Ahn IS, Diamante G, Zhang G, Thorson A, Schaefers KP, Stafford JM, Yang X.
Biol Sex Differ. 2026 Feb 23;17(1):41. doi: 10.1186/s13293-026-00859-z.
PMID: 41731620 Free PMC article.