Media Coverage

AsymAD: Why Some Brains with Alzheimer’s Stay Sharp — New Insights into Cognitive Resilience

April-May 2026 | UC San Diego Today • Infobae • San Diego Union-Tribune/La Jolla Light • ScienceAlert • Futura

Research led by investigators at UC San Diego uncovered new insights into asymptomatic Alzheimer’s disease (AsymAD)—a condition in which individuals remain cognitively intact despite Alzheimer’s disease-related brain pathology.

Combining large-scale human transcriptomic analysis, AI-guided Boolean network modeling, and experimental validation, the researchers identified a molecular signature that distinguishes normal aging, symptomatic Alzheimer’s disease, and asymptomatic disease. The work identified chromogranin A (CgA) as a potential molecular regulator associated with cognitive vulnerability or resilience in the presence of Alzheimer’s-related pathology.

The study also established a murine model of AsymAD, providing an experimental platform for investigating mechanisms of cognitive resilience and identifying potential therapeutic strategies for preserving cognitive function despite underlying neuropathology. The work was published in Acta Neuropathologica Communications.

Featured Publication:
Jati S, Taheri S, Kal S, Sinha SC, Head BP, Mahata SK, Sahoo D. AI-guided discovery of a murine model of asymptomatic Alzheimer's disease. Acta Neuropathologica Communications. 2026;14(1):110.

Featured Media

UC San Diego Today | April 20, 2026
Why Some Brains with Alzheimer’s Stay Sharp

The UC San Diego Research Alert highlighted the discovery of molecular mechanisms that may help explain why some individuals remain cognitively healthy despite Alzheimer’s-related brain changes.

Infobae | April 21, 2026
Why Some People with Alzheimer’s Remain Lucid and Show No Symptoms

The international feature highlighted biological mechanisms that may help explain why some individuals remain cognitively intact despite Alzheimer’s-related neuropathology. Sushil K. Mahata, Ph.D., a senior author of the study, spoke with Infobae about the findings and their potential implications for understanding cognitive resilience.

San Diego Union-Tribune / La Jolla Light | April 24, 2026

“This Is a Huge Finding”: UCSD Researchers Work on Way to Prevent Alzheimer’s Disease with Molecular “Switch”

The feature explored the history behind the CgA research, the discovery of cognitive resilience in the mouse model, and the potential implications of investigating resilience mechanisms rather than focusing solely on established disease.

ScienceAlert | April 28, 2026
Scientists Discover a Key Difference in Brains That Resist Alzheimer’s

ScienceAlert highlighted the identification of CgA as a potential link between Alzheimer’s-associated brain pathology and cognitive decline, as well as the development of the AsymAD mouse model for further investigation.

Futura | May 11, 2026
Alzheimer’s Resilience Gene: Why 30% of People Avoid Dementia Despite Brain Damage

Futura discussed the study’s Boolean network modeling, 40-gene molecular signature, CgA-centered mechanism, and sex-dependent differences in resilience observed in the experimental model.

Melanoma: Catestatin Emerges as a Potential Strategy Against Melanoma and Drug Resistance

May-June 2026 | UC San Diego Today • Medical Xpress/MSN • StudyFinds

Research led by investigators at UC San Diego identified a potential new therapeutic application for catestatin (CST) in melanoma. In preclinical studies, CST reduced melanoma growth and tumor burden, suppressed tumor-cell migration and invasive behavior, and reprogrammed molecular pathways associated with tumor progression and resistance to targeted therapy.

Importantly, CST demonstrated activity in drug-resistant melanoma cells and reduced melanoma-cell viability while sparing normal skin cells under the experimental conditions. Endogenous CST levels also declined with advancing melanoma stage, suggesting a potential relationship between reduced CST and disease progression.

Featured Publication:

Kal S, Jati S, Tang K, Webster NJG, Corti A, Mahata SK. Catestatin peptide impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways. Oncogenesis. 2026;15(1):39.

Featured Media

UC San Diego Today | May 27, 2026
Naturally Occurring Molecule May Help Outsmart Melanoma

The UC San Diego Research Alert highlighted CST as a naturally occurring CgA-derived peptide that slowed melanoma growth, reduced the ability of melanoma cells to spread, and restored sensitivity in drug-resistant melanoma cells. The findings support further investigation of CST as the basis for peptide-based approaches to advanced and therapy-resistant melanoma.

The article also featured Sushil K. Mahata, Ph.D., co-senior author of the study, discussing CST’s ability to disrupt pathways associated with therapeutic resistance and shift melanoma cells toward a more treatment-sensitive state.

StudyFinds | June 10, 2026

Melanoma May Have a Natural Enemy: A Tiny Protein Fragment the Human Body Already Produces

StudyFinds provided an in-depth independent analysis of the research, highlighting CST’s effects on melanoma growth, tumor-cell survival and migration, and resistance to targeted therapy. The report emphasized that CST reduced melanoma-cell viability while leaving normal skin cells unaffected in the experimental systems.

The feature also examined CST’s activity in vemurafenib-resistant melanoma cells, including its effects on molecular programs associated with drug resistance. The article appropriately noted that the findings remain preclinical and that CST has not yet been tested as a melanoma therapy in humans.

Medical Xpress / MSN | 2026
Naturally Occurring Molecule May Help Outsmart Melanoma

Medical Xpress coverage, distributed through MSN, highlighted the discovery that CST significantly slowed melanoma growth, reduced melanoma-cell migration and invasive behavior, and restored sensitivity in drug-resistant melanoma cells, supporting further investigation of peptide-based approaches for advanced and treatment-resistant melanoma.

Cardiometabolic Disorders: Catestatin Improves Glucose Homeostasis and Insulin Sensitivity in Obesity

February 2018 | UC San Diego Today • EurekAlert!

Research from UC San Diego School of Medicine highlighted the therapeutic potential of catestatin (CST) in obesity and type 2 diabetes. In preclinical studies, CST treatment improved glucose tolerance and insulin sensitivity and reduced body weight in obese mice. The study also identified important roles for CST in regulating hepatic inflammation, macrophage recruitment, glucose production, and insulin resistance.

CST treatment reduced the recruitment of inflammatory macrophages to the liver, decreased inflammation, lowered elevated glucose and insulin levels, and reduced hepatic lipid accumulation in obese mice. These findings provided early evidence supporting CST as an endogenous regulator of metabolic homeostasis and established a foundation for subsequent therapeutic development in obesity, insulin resistance, and related metabolic disorders.

Featured Publication:

Ying W, Mahata S, Bandyopadhyay GK, et al. Catestatin inhibits obesity-induced macrophage infiltration and inflammation in the liver and suppresses hepatic glucose production, leading to improved insulin sensitivity. Diabetes. 2018;67(5):841-848.

Featured Media

UC San Diego Today | February 7, 2018
Peptide Improves Glucose and Insulin Sensitivity, Lowers Weight in Mice

The UC San Diego feature highlighted the study’s findings suggesting potential applications of CST in obesity and type 2 diabetes.

The article also featured Sushil K. Mahata, Ph.D., senior author of the study, discussing CST’s direct suppression of hepatic glucose production and its effects on hepatic lipid accumulation and macrophage-mediated inflammation in obese mice.

EurekAlert! | February 8, 2018
Peptide Improves Glucose and Insulin Sensitivity, Lowers Weight in Mice

The news release highlighted the study’s findings on CST-mediated improvements in glucose metabolism, insulin sensitivity, inflammation, and body weight in preclinical models of obesity.