2025년 뇌 질환 신경생물학상

The McKnight Endowment Fund for Neuroscience has selected four projects to receive the 2025 Neurobiology of Brain Disorders Awards. The awards will total $1.2 million for research on the biology of brain diseases, with each project receiving $100,000 per year in each of the next three years for a total of $300,000 funded per project.

NBD (Neurobiology of Brain Disorders)상은 신경 및 정신 질환을 연구하는 미국 과학자들의 혁신적인 연구를 지원합니다. 이상은 뇌와 신경계에 대한 실험실 발견을 인간의 건강을 개선하기위한 진단 및 치료법으로 전환하기 위해 기본 및 임상 신경 과학 간의 협력을 장려합니다.

추가적인 관심 분야는 환경이 뇌 장애에 미치는 영향입니다. 어린 시절의 환경적 스트레스는 나중에 신경학적, 정신적 장애를 일으키는 강력한 처분 요인입니다. 연구에 따르면 유색 인종 공동체는 환경(예: 기후, 영양, 화학 물질 노출, 오염)부터 사회(예: 가족, 교육, 주택, 빈곤)에 이르는 다양한 스트레스 요인에 걸릴 위험이 더 높습니다. 임상적 관점에서 환경 요인이 뇌 질환에 어떻게 영향을 미치는지 이해하는 것은 효과적인 치료법을 개발하는 데 필수적입니다.

“From decoding the complex mechanisms that underlie neurodegeneration to charting the circuitry of pain and uncovering how paternal exposures shape brain health, the researchers selected for this year’s award are pushing the frontiers of neuroscience in bold and necessary directions,” said Michael Ehlers, M.D., Ph.D., Chair of the Awards Committee and Entrepreneur Partner at MPM BioImpact. “This year’s projects include investigations into the higher-order interactome in C9orf72-mediated ALS, myelin dysfunction in Alzheimer’s disease, the spinal output map of pain states, and, for the first time since announcing our emphasis two years ago, an environmentally focused project examining how paternal stress impacts offspring neurobiology. These efforts promise to reshape our understanding of brain disease and point to transformative therapeutic possibilities for the future.”

이 상은 1953년 McKnight 재단을 설립하고 뇌 질환 연구를 지원하고자 했던 William L. McKnight의 관심에서 영감을 받았습니다. 그의 딸인 Virginia McKnight Binger와 McKnight 재단 이사회는 1977년 그를 기리기 위해 McKnight 신경과학 프로그램을 설립했습니다.

매년 여러 상이 수여됩니다. 올해의 4개상은 다음과 같습니다.

With 182 letters of intent received this year, the awards are highly competitive. A committee of distinguished scientists reviews the letters and invites a select few researchers to submit full proposals. In addition to Dr. Ehlers, the committee includes Nicole Calakos, M.D., Ph.D., Duke University; Gloria Choi, Ph.D., Massachusetts Institute of Technology; André Fenton, Ph.D., New York University; Joseph G. Gleeson, M.D., University of California San Diego; Tom Lloyd, M.D., Ph.D., Baylor College of Medicine; and Michael Shadlen, M.D., Ph.D., Columbia University.

Applications for both the 2026 Neurobiology of Brain Disorders Awards and Scholar Awards open August 1, 2025.

신경 과학을위한 McKnight 기금 기금 소개

The McKnight Endowment Fund for Neuroscience is an independent organization funded solely by the McKnight Foundation of Minneapolis, Minnesota, and led by a board that includes prominent neuroscientists from around the country. The McKnight Foundation has supported neuroscience research since 1977. The Foundation established the Endowment Fund in 1986 to carry out one of the intentions of founder William L. McKnight (1887–1978), one of the early leaders of the 3M Company.

뇌 장애의 신경생물학상 외에도 기부 기금은 McKnight Scholar Awards를 통해 연례 시상 자금을 제공하여 연구 경력의 초기 단계에 있는 신경과학자들을 지원합니다.

뇌 장애 상 신경 생물학 상

Hyejung Won, Ph.D., Associate Professor, Genetics, University of North Carolina School of Medicine, and co-principal investigator David Shechner, Ph.D., Assistant Professor, Pharmacology, University of Washington, Seattle, Washington

Deciphering the higher-order interactome in C9orf72-mediated ALS

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive loss of motor neurons and muscle weakness. Inherited forms of ALS are often linked to abnormal expansions of short DNA sequences—known as short tandem repeats (STRs)—in the C9orf72 gene. Despite this clear genetic link, developing effective therapies for C9orf72-mediated ALS has been challenging due to the complexity of its underlying mechanisms.

C9orf72-mediated ALS involves multiple disease processes, including toxic RNA and protein buildup. Emerging evidence also suggests that STR expansions may disrupt how DNA is packaged in cells, but the exact molecular mechanisms remain poorly understood. Drs. Hyejung Won and David Shechner aim to apply cutting-edge genetic and chemical biology tools to uncover how C9orf72 STR expansions reshape the DNA architecture and contribute to ALS pathology.

Upasna Sharma, Ph.D., Assistant Professor, Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, California

Paternal environmental contributions to stress dysregulation in offspring

Can a father’s exposure to stress shape the biology of his children? Emerging evidence suggests it can. Epidemiological studies link paternal stress and adverse life experiences to increased risk of neuropsychiatric disorders in offspring, yet the mechanisms remain poorly understood. Dr. Sharma’s research aims to address this gap by investigating how chronic stress in male mice alters sperm and programs stress dysregulation in offspring.

Her lab found that male—but not female—offspring of stressed fathers exhibit blunted stress responses, a trait associated with certain psychiatric disorders. Dr. Sharma aims to uncover the molecular signals behind such inheritance, focusing on small RNA molecules in sperm. Her lab will dissect how stress signals are communicated from the brain to sperm and how these signals influence early development to affect offspring health. This research aims to offer new insight into the biological roots of stress-related disease risk.

Allan-Hermann Pool, Ph.D., Assistant Professor, Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas

Characterization and therapeutic targeting of the spinal output map of pain states

Pain is a motivational system that forces us to avoid physical harm converting detection of injuries to adaptive avoidance, coping and learning behaviors. While pain is important for survival, compromised pain processing can lead to chronic pain which remains a formidable public health burden. The cellular substrates that cause central persistent pain states and means to selectively therapeutically control them remain poorly defined. In previous work, the Pool lab has identified spinal cord neuronal repertoires that are driven by diverse surface and deep tissue injuries identifying candidate neural substrates for pain.

In new work, the Pool lab aims to elucidate the causal role of pain engaged spinal cord circuit nodes in pain processing. Furthermore, they seek to develop a new immunotoxin based strategy to locally eliminate pain mediating spinal cord cell populations and thereby deliver a modular single-administration therapeutic solution for pain management.

Brad Zuchero, Ph.D., Assistant Professor, Neurosurgery, Stanford University, Stanford, California, and co-principal investigator Ethan Hughes, Ph.D., Associate Professor, Cell & Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, Colorado

Does myelin dysfunction drive Alzheimer’s disease?

Myelin is required for rapid and precise nerve signaling and plays essential roles in neuroprotection, learning, and memory. Myelin dysfunction and loss have emerged as early hallmarks of neurodegenerative diseases, including Alzheimer’s disease (AD). However, the cellular mechanisms driving myelin dysfunction and loss in AD remain largely unknown.

Together, the Zuchero and Hughes lab will use a rigorous mouse genetics-driven myelin phenotyping pipeline to define the effects of key AD-linked genes on myelin formation and integrity. The project will leverage the complementary expertise of the Zuchero lab in myelin cell biology and genetic tool building, and the Hughes lab in longitudinal in vivo imaging of myelin formation/dynamics and behavioral assessments.

Overall, this project seeks to open up an emerging area of AD research that may reveal myelin as a new, untapped therapeutic target—a transformative research goal that the Zuchero and Hughes labs are poised to tackle together.