The McKnight Endowment Fund for Neuroscience has selected four projects to receive the 2026 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 uncovering how physiological temperature reshapes pain signaling, to mapping circuits that connect early life adversity to fear, to restoring motor plasticity in the aging brain, the researchers selected for this year’s award are pushing the frontiers of neuroscience in bold and much needed directions,” said Michael Ehlers, M.D., Ph.D., Chair of the Awards Committee. This year’s projects include investigations into temperature as a missing variable in pain biology and drug discovery, the development of septal dopamine circuits controlling fear in the context of early life stress, the rescue of cortical plasticity and motor learning in aging, and an environmentally focused project examining how early life high fructose exposure impairs microglial function and disrupts neurodevelopment. 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 177 applications 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 Nancy Bonini, Ph.D, University of Pennsylvania; Nicole Calakos, M.D., Ph.D., Duke University; Gloria Choi, Ph.D., Massachusetts Institute of Technology; Joseph G. Gleeson, M.D., University of California San Diego; Evan Macosko, M.D., Ph.D., Broad Institute of 매사추세츠 공과 대학 and Harvard University; and Michael Sofroniew, Ph.D., M.D., University of California, Los Angeles.
Applications for both the 2027 Neurobiology of Brain Disorders Awards and Scholar Awards open August 3, 2026, and will be accepted through October 15 and November 3, 2026, respectively.
신경 과학을위한 McKnight 기금 기금 소개
맥나이트 신경과학 기금(McKnight Endowment Fund for Neuroscience)은 미네소타주 미니애폴리스에 있는 맥나이트 재단(McKnight Foundation)의 단독 기금으로 운영되는 독립 기관으로, 전국의 저명한 신경과학자들이 포함된 이사회가 이끌고 있습니다. 맥나이트 재단은 1977년부터 신경과학 연구를 지원해 왔습니다. 3M의 초기 경영자 중 한 명이었던 설립자 윌리엄 L. 맥나이트(1887–1978)의 의도 중 하나를 실현하기 위해 1986년에 기금을 설립했습니다.
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

Juan Du, Ph.D., Professor, Northwestern University, Evanston, IL
Temperature as a Missing Dimension in Pain Neurobiology and Therapy
Temperature is one of the most fundamental signals sensed by the nervous system, shaping experiences from the warmth of sunlight to the pain of touching a hot surface. The Du laboratory studies how the body detects temperature and how disruptions in these pathways contribute to neurological disorders.
Recent discoveries from the Du laboratory suggest that temperature is a previously overlooked “missing dimension” in biomedical research and drug discovery. Most biological experiments and drug screenings are performed at room temperature, even though proteins function in the body at 37°C. The lab discovered that important protein states and drug interactions can remain hidden under conventional laboratory conditions and only emerge at body temperature. These findings may help explain why some drug candidates succeed in early studies but fail later in development. Through this project, the team aims to uncover how temperature-driven protein dynamics contribute to chronic pain and to develop “temperature-aware” therapies with greater precision and fewer side effects.

Corey Harwell, Ph.D., Professor, University of California, San Francisco, San Francisco, CA
How Early Life Stress Shapes the Development of Septal Dopamine Circuits Controlling Fear
Anxiety disorders affect millions of people worldwide, and early life stress is one of the strongest risk factors for developing anxiety and trauma-related disorders later in life. Despite this clear link, the mechanisms by which stressful experiences during childhood alter the developing brain remain poorly understood. Emerging evidence suggests that disruptions in dopamine circuits involved in fear, safety learning, and emotional regulation may contribute to long-lasting changes in behavior.
The Harwell lab aims to determine how early life stress alters the development of a specific dopamine circuit connecting the ventral tegmental area and lateral septum, two brain regions involved in regulating fear and anxiety-related behaviors. Using advanced genetic, imaging, and behavioral approaches in mice, the lab will define how stress changes the maturation and activity of this circuit and whether these alterations impair the ability to recognize when danger has passed. Overall, this work could identify new therapeutic targets and developmental windows for treating anxiety and trauma-related disorders.

Takaki Komiyama, Ph.D., Professor, University of California, San Diego, San Diego, CA
Rescuing Motor Learning Failure in Aging
The brain continuously reshapes itself through experience, allowing people to learn new skills, adapt to changing environments, and recover from challenges. Yet this remarkable flexibility is not unlimited. As we age and in many neurological conditions, the brain circuits become less able to reorganize itself in an adaptive manner, making learning and recovery increasingly difficult. Takaki Komiyama’s research seeks to uncover the fundamental rules that allow the brain to remain adaptable throughout life and to understand why those mechanisms sometimes fail.
His laboratory combines innovative approaches that allow researchers to observe and precisely influence the activity of individual neurons in the brains of behaving animals. By studying how experiences alter neural circuits, his team aims not only to reveal how learning naturally occurs, but also to determine whether the brain’s ability to change can be restored or enhanced when it becomes impaired. This work seeks to bridge fundamental discoveries about how the brain learns with future strategies to improve learning, recovery, and brain health across the lifespan.

Justin Perry, Ph.D., Associate Member, Memorial Sloan Kettering Cancer Center, New York, NY
Understanding How Early Life High Fructose Exposure Suppresses Microglia Efferocytosis and Disrupts Neurodevelopment
Despite its success as a low-cost food additive, there has been significant attention on the potential downsides to the dramatic increase in use of high fructose corn syrup across the world, especially in foods marketed to children. Emerging evidence suggests that high fructose consumption by pregnant mothers (via breast milk) or by adolescent children is associated with the development of mood, anxiety, and autism spectrum disorders during adolescence. Despite this emerging link and the growing prevalence of such disorders, very little is known about how high fructose exposure affects neurodevelopment.
During development, the human brain not only massively expands the number of new neurons formed but must also remove neurons that are deemed surplus. This process is achieved by specialized cells, called microglia, who must manage this burdensome but essential process in the harsh environment of the developing brain. Dr. Perry aims to apply cutting-edge approaches from multiple fields to uncover the metabolic pathways that support phagocytosis by microglia and to understand why these pathways go awry when the brain is exposed to high fructose.



