Bradley Goldstein
Duke University, NC·Neuroscience
Smell begins in a thin sheet of tissue high in the nose, the olfactory epithelium, which holds millions of sensory neurons that send signals directly to the brain. Infection, inflammation, toxins or head injury can damage this tissue and leave people with no sense of smell, a reduced one, or distorted odor perception.
- Fields
Neuroscience
Medicine & Clinical Research
Genetics
- Topics
olfaction
sense of smell
olfactory epithelium
- Grants
- 2 known grants, through Jul 2029
What they work on
- Map the axes of gene-expression variation across human olfactory sensory neurons by single-cell RNA sequencing of nasal biopsies from people with normal smell and from people with objectively measured smell loss.
- Read odor responses one cell at a time in the living human nose using Act-seq, presenting a defined odorant before biopsy to identify which neurons responded, and so match human odor receptors to their odors.
- Compare Act-seq odor responses between people with normal smell and people whose smell loss followed COVID-19, to see how odor-evoked neuronal activity is altered in disease.
- Profile olfactory neurons, their progenitor cells and supporting cells by single-cell RNA sequencing in preclinical and symptomatic Alzheimer's subjects from a Duke/UNC research center cohort, stratifying by sex, race and APOE-e4 status.
- Define how immune cell populations in the olfactory lining and their gene expression change across Alzheimer's disease stages, and test olfactory cell function in vitro.
More about the research
Despite how common this is — most visibly in the millions who lost smell after COVID-19 — there are no effective treatments, and the basic biology of smell loss in humans is poorly understood. Both projects address this gap using a minimally invasive nasal biopsy combined with single-cell profiling, one asking how human olfactory neurons normally work and fail, the other asking what smell loss reveals about Alzheimer's disease.
Why it matters
Millions of people have lasting smell loss after COVID-19 or other insults, and no treatment exists; smell loss is also one of the earliest signs of Alzheimer's disease. Defining what goes wrong in human olfactory neurons and their supporting and immune cells could supply targets for therapies aimed at restoring smell, and could inform whether nasal tissue serves as an accessible window on early Alzheimer's progression. The resulting single-cell datasets would be available to other researchers.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Minghong Ma
Johns Hopkins University, MD·Neuroscience
Test whether olfactory epithelium inflammation or smell-neuron inactivation from adolescence to adulthood alters prefrontal pyramidal neurons in mice, using patch clamp recordings, and reverse effects with chemogenetic activation of olfactory-prefrontal circuits.
Jonathan Overdevest
Columbia University, NY·Medicine & Clinical Research·Early-career
Identify epidemiologic risk factors for initial and persistent olfactory dysfunction after COVID-19 in a multi-ethnic patient cohort, using both self-reported and test-based smell measures.
Kevin Franks
Duke University, NC·Neuroscience
Test whether piriform cortex neurons jointly encode olfactory bulb input and breathing phase, by delivering brief optogenetic light pulses to different olfactory bulb spots timed to respiration in awake, head-fixed mice.
The school
Duke University: 61 labs on PI Pages, $1.6B a year on research, 417 research doctorates a year.
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