Jacob Labonte,BS,and Michael L Alosco,PhD,are the recipients of the 2026 Alzheimer Award

The Journal of Alzheimer’s Disease (JAD) is pleased to announce that Jacob Labonte, BS, and Michael L Alosco, PhD, are the recipients of the 2026 Alzheimer Award. The award is presented by the journal in recognition of Labonte, Alosco and colleagues’ groundbreaking article “Sex differences on tau, astrocytic, and neurodegenerative plasma biomarkers”. ¹ The awardee is selected by the journal’s Editorial Board from the 2025 year’s volume (over 800 papers), and is presented with the Alzheimer Medal, a 3" bronze medal with the likeness of Alois Alzheimer, and a cash prize of $7,500. The 2026 award is proudly sponsored by Sage Publications (www.sagepub.com).

Jacob Labonte, BS, received his Bachelor of Science in Biology from Worcester State University in Worcester, MA. After graduating, he became employed at the Boston University Alzheimer’s disease and CTE Research Centers, initially working as a Clinical Research Assistant, now the Research Program Manager. His research interests focus on investigating health disparities and social determinants of health related to sex, gender, race, and sexuality. This was his first publication as the first author. He intends to pursue graduate school to develop his training and knowledge further and continue contributing to research and clinical care in Alzheimer’s disease and neurodegenerative diseases.

Jacob’s pursuit of Alzheimer’s disease research is in honor of his grandfather, Michael Cellere, who passed away in 2025 with early-onset AD.

Michael L Alosco, PhD, is a clinical neuropsychologist and Research Vice Chair & Professor of Neurology at the Boston University Chobanian & Avedisian School of Medicine, where he serves as the Leader of the Boston University Alzheimer’s Disease Research Center Clinical Core and the Co-Director of Clinical Research at the BU CTE Center. He directs Neuropsychology for the Boston Medical Center Memory & Aging Clinic, an evaluation site for the BU ADRC, and serve as Site PI for the Alzheimer’s Disease Neuroimaging Initiative and CLARiTI. He has an established research program that has a focus on: (1) the development of in vivo biomarkers for AD and AD related dementias (ADRD) with a focus on plasma biomarkers; (2) the contribution of cerebrovascular disease to the clinical and neuropathological expression of AD/ADRD; and (3) the relationship between repetitive traumatic brain injuries (TBIs) with cognitive and neuropsychiatric decline, and neurodegenerative disease(s). He has >270 peer-review publications; is the contact PI of several R01s that are investigating MRI, plasma, and cerebrospinal fluid biomarkers of AD/ADRD. His research in the field of AD/ADRD has led to high impact publications, setting the stage for risk of late neurological disorders due to RHI and for CTE biomarker discovery. Through his funded research program, he has extended the infrastructure to study the late effects of RHI and CTE to several other Centers in the U.S. He hopes his work will ultimately lead to the development of strategies to diagnose, treat and prevent CTE and Alzheimer’s disease.

Importance of published article

The association between female sex and increased risk of Alzheimer’s disease (AD) has been well established. Sex differences have been found at autopsy, neuroimaging, and cerebrospinal fluid outcomes related to AD. However, the mechanisms that cause females to disproportionately experience AD remain unclear.

In an effort to investigate this association, this study examined sex differences on cross-sectional and longitudinal levels of plasma glial fibrillary acidic protein (GFAP), neurofilament light (NfL), phosphorylated tau (p-tau₁₈₁), and total tau (t-tau) among 567 participants from the Boston University Alzheimer’s Disease Research Center who spanned the diagnostic continuum. We found that females had higher plasma GFAP compared to males at baseline, regardless of cognitive diagnosis. Among those with dementia, females had higher plasma NfL levels compared to males. Plasma NfL selectively predicted accelerated progression of dementia severity in females but not males. There were no significant findings for plasma p-tau₁₈₁ and t-tau.

This study found distinct sex-related differences in blood-based biomarkers of tau, neuroinflammation, and neuronal injury, providing further insights into the potential pathways by which female sex confers risk for AD. Understanding the mechanisms responsible for these differences is imperative in developing AD biomarkers, diagnostic, and prognostic strategies that can benefit all, including those who have historically been disproportionately affected. The study encourages the need for additional research that incorporates and evaluates biological factors of sex, such as sex hormones, menstrual and reproductive health. Furthermore, there remains a need to establish studies that appropriately distinguish between factors of sex and gender.