Osvaldo Delbono
Wake Forest University, NC·Neuroscience
As people age, their muscles shrink and weaken, a condition called sarcopenia. In Alzheimer's disease (AD), muscle loss can begin years before memory problems or brain shrinkage.
- Fields
Neuroscience
Physiology
Medicine & Clinical Research
- Topics
sarcopenia
aging
Alzheimer's disease
- Grants
- 2 known grants, through Nov 2028
What they work on
- Define how brainstem A5 sympathetic neurons projecting to hindlimb muscles affect motor denervation, neuromuscular junction signaling and muscle mass and strength with aging, using optogenetics and retrograde labeling in living mice.
- Test whether sustained expression of Phox2b, a master gene regulator of sympathetic neurons, in A5 hindlimb-projecting neurons reduces age-related loss of sympathetic and motor nerve supply to muscle.
- Determine how A5 hindlimb-projecting neurons contribute to muscle denervation, reduced norepinephrine release at the neuromuscular junction and weaker adrenoceptor signaling across early, middle and late stages of Alzheimer's disease in mice.
- Test whether turning A5 hindlimb-projecting neurons up with chemogenetics, designer receptors controlled by drugs, at different Alzheimer's stages restores muscle innervation and delays or reverses accelerated sarcopenia.
More about the research
This raises the question of whether the brain's control of muscle fails early. Both projects focus on a small brainstem cluster, the A5 nucleus. Its neurons use the chemical messenger norepinephrine and send signals through the spinal cord to the sympathetic nervous system (SNS), the body's "fight-or-flight" network. The team calls the A5 neurons that reach the hindlimb muscles SNPHLM. The lab proposes that damage to these neurons drives muscle loss in both normal aging and early AD.
Why it matters
Sarcopenia reduces strength and independence in older adults, and muscle loss may be an early sign of Alzheimer's disease. Showing that brainstem sympathetic neurons control muscle could shift sarcopenia treatment targets from muscle to the nervous system. It could also help detect Alzheimer's before dementia appears and guide treatments matched to each disease stage.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Bumsoo Ahn
Wake Forest University, NC·Physiology·Early-career
Test whether unacylated ghrelin (UnAG) combined with endurance exercise boosts mitochondrial energy production and lowers oxidative stress in skeletal muscle of older mice, compared with either treatment alone.
Robert Carrillo
University of Chicago, IL·Neuroscience·Early-career
Test how combinations of Dpr and DIP cell surface proteins tell Drosophila motor neurons which muscles to connect to, using single-cell genetic changes in motor neurons that express six DIPs.
Clarissa Henry
University of Maine, ME·Biology
Determine motor neuron- and muscle-specific roles for Dol-P-Man, a sugar building block made with the help of Dpm3, and dystroglycan (DG) at the neuromuscular junction, using cell-type-specific zebrafish genetic models.
The school
Wake Forest University: 27 labs on PI Pages, $345M a year on research, 54 research doctorates a year.
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