Daniel David

Faculty

Daniel David headshot

Daniel David

PhD RN

Assistant Professor

1 212 992 5930

433 First Ave
New York, NY 10010
United States

Accepting PhD students

Daniel David is a geriatrics and palliative care (PC) nurse researcher and an Assistant Professor at the Rory Meyers College of Nursing at New York University. As an implementation scientist, he seeks to translate nursing research into feasible, effective, and scalable interventions for under-resourced, community-dwelling older adults and their care partners who are on the cusp of needing nursing home care.

His research program addresses the unmet social, emotional, and serious illness needs of low-income residents living in Medicaid-supported assisted living (AL) facilities in New York City. Notably, he developed the “Someone to Talk To” program in partnership with a community advisory board of AL residents. This initiative pairs residents with community health workers to foster serious illness conversations, explore values and care goals, and bridge care gaps for isolated individuals at high risk of nursing home placement. This work has been recognized nationally through the Center to Advance Palliative Care (CAPC) Tipping Point Challenge (Silver Medal) and internationally by the Gerontological Society of America (GSA) Distinguished Nursing Research Manuscript Award.

David serves on the editorial board of the Journal of the American Geriatrics Society (JAGS), the advisory council of the American Assisted Living Nurses Association (AALNA), and the research core of the Center of Excellence for Assisted Living (CEAL-UNC). He has received career development awards from the Cambia Foundation and the National Palliative Care Research Center (NPCRC).

Beyond his primary research focus in assisted living, David has served as a Co-Investigator on NIH-funded projects, including a study on the experiences of New York City hospice team members during the COVID-19 pandemic (5R01NR019792). He is currently a Site Principal Investigator at NYU Langone Medical Center for a 40-site trial examining a nurse-led intervention aimed at reducing avoidable hospitalizations among patients living with dementia and their care partners (U19AG078105). Collectively, his research promotes person-centered and community-based approaches to improving care for older adults with serious illnesses.

PhD - Northeastern University
BSN - University of Virginia
MS - University of Colorado

Gerontology
Palliative care

American Geriatrics Society
Gerontological Society of America
Hospice and Palliative Nurses Association
Palliative Care Research Cooperative
Sigma Theta Tau

Junior Investigator, Palliative Care Research Consortium (2018)
VA Quality Scholar, VA Medical Center, San Francisco (2018)
Scholarship, End of Life Nursing Education Consortium (2017)
Sigma Theta Tau, Scholar Research Award, Northeastern University (2016)
Kaneb Foundation Research Award, Regis College (2015)
Scholar, Summer Genetics Institute, NINR, National Institute of Health (2014)
Scholar, Jonas Center for Nursing Excellence (2014)
Sigma Theta Tau, Rising Star Award, Northeastern University (2013)
Sigma Theta Tau, Beta Kappa (2004), Gamma Epsilon Chapter (2013)
Distinguished Nursing Student Award, University of Virginia (2005)
Raven Society, University of Virginia (2005)

Beneficial effects of intraventricularly administered BMP-7 following a striatal 6-hydroxydopamine lesion

Zuch, C. L., David, D., Ujhelyi, L., Hudson, J. L., Gerhardt, G. A., Kaplan, P. L., & Bickford, P. C. (2004). Brain Research, 1010(1), 10-16. 10.1016/j.brainres.2003.12.058
Abstract
Abstract
The present study was undertaken to investigate the effects of bone morphogenetic protein-7 (BMP-7), also named osteogenic protein-1 (OP-1), on the progression of a striatal 6-hydroxydopamine (6-OHDA) lesion. BMP-7, a member of the transforming growth factor-β (TGF-β) superfamily of proteins, has been shown to have protective effects in other animal models of neuronal damage. In this study, male Fischer 344 rats received striatal 6-OHDA lesions followed 1 week later by an intraventricular dose of BMP-7. No significant effect of BMP-7 treatment on spontaneous locomotor activity was observed, however BMP-7 significantly increased the density of tyrosine hydroxylase (TH) immunoreactivity (TH-ir) in the substantia nigra (SN) pars compacta, in the lesioned hemisphere [31.7±5.2 (optical density (O.D.) arbitrary units) control vs. 50.2±4.3 O.D. BMP-7-treated; p<0.05]. Interestingly, BMP-7 significantly increased TH-ir in the SN of the non-lesioned hemisphere (pars reticulata: 14.8±1.19 O.D. control vs. 36±2.6 O.D. BMP-7-treated, p<0.05; pars compacta: 29.0±4.9 O.D. control vs. 64.4±6.9 O.D. BMP-7-treated, p<0.001). A significant increase in DA concentration in the contralateral, non-lesioned hemisphere was also noted (113.2 ng/g control vs. 198.2 ng/g BMP-7-treated, p<0.01). In contrast to other intraventricularly administered neurotrophic factors, BMP-7 was not associated with an increase in the sensitivity to pain. These results suggest that BMP-7 is able to act as a dopaminotrophic agent without unwanted side effects and as such may be a useful pharmacological tool in the treatment of Parkinson's disease in humans.

In vivo electrochemical studies of dopamine clearance in subregions of rat nucleus accumbens: Differential properties of the core and shell

David, D. J., Zahniser, N. R., Hoffer, B. J., & Gerhardt, G. A. (1998). Experimental Neurology, 153(2), 277-286. 10.1006/exnr.1998.6898
Abstract
Abstract
The dopamine (DA) uptake/clearance properties of the DA transporter (DAT) in the core and shell of the nucleus accumbens were measured using in vivo electrochemical recordings. Calibrated amounts of a DA solution were pressure-ejected from a micropipette/ electrode assembly placed in the core or shell of the nucleus accumbens in anesthetized male Fischer 344 rats. Initial studies in the two brain regions revealed that the core and shell have different DA clearance properties as measured by the extracellular DA signal amplitudes, clearance times, and clearance rates. Although the same number of picomoles of DA were applied, DA clearance signals recorded in shell had significantly greater amplitudes but faster clearance rates than those recorded in the core. Systemic administration of 20 mg/kg cocaine, a monoamine transporter inhibitor, greatly increased the signal amplitude from the locally applied DA in both the core and shell. Signal amplitudes were increased to a greater extent in the shell, compared with the core, after cocaine administration. However, cocaine affected the clearance time of DA only in the core and the DA clearance rate only in the shell. Taken together with previously reported data, these studies further support differential activity of the DAT in the core versus shell subregions of the nucleus accumbens. In addition, these data indicate that DATs are more sensitive to the effects of psychomotor stimulants, such as cocaine, in the shell of the nucleus accumbens.

Nicotine-evoked nitric oxide release in the rat hippocampal slice

Smith, D. A., Hoffman, A. F., David, D. J., Adams, C. E., & Gerhardt, G. A. (1998). Neuroscience Letters, 255(3), 127-130. 10.1016/S0304-3940(98)00725-3
Abstract
Abstract
The effects of cholinergic agonists on nitric oxide (NO) release in hippocampal slices from male Sprague-Dawley rats were investigated using electrochemical recording procedures using Nafion and o-phenylenediamine- treated carbon fiber microelectrodes. These microelectrodes are highly selective for NO versus other interferents. Acetylcholine (Ach) with neostigmine, or nicotine was delivered by pressure ejection from pipettes placed within 300 μm of the NO sensors. Both Ach arid nicotine produced NO signals ranging from 0.04 to 2.14 μM in the CA1, CA3, and dentate gyrus of the rat hippocampus that lasted for 2-5 min. The Ach responses were not antagonized by the muscarinic antagonist atropine. However, nicotine-evoked responses were partially antagonized by α-bungarotoxin, a finding consistent with α7-nicotinic cholinergic receptors being involved with the effects of nicotine. These data support the hypothesis that nicotine is capable of evoking long lasting NO release in the hippocampus.

6-Hydroxydopamine induces the loss of the dopaminergic phenotype in substantia nigra neurons of the rat. A possible mechanism for restoration of the nigrostriatal circuit mediated by glial cell line-derived neurotrophic factor

Bowenkamp, K. E., David, D., Lapchak, P. L., Henry, M. A., Granholm, A. C., Hoffer, B. J., & Mahalik, T. J. (1996). Experimental Brain Research, 111(1), 1-7.
Abstract
Abstract
Intraparenchymal injections of the neurotoxin 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle in rats destroys the dopaminergic neurons in the pars compacta of the substantia nigra. In other transmitter systems it has been found that axotomy or neurotoxin exposure produces an initial loss of neurotransmitter phenotype, with cell death occurring over a much slower time course. To determine whether this also occurs in dopamine neurons after 6-OHDA, two approaches were utilized. First, the effect of injections of 6-OHDA into the medial forebrain bundle on nigral dopaminergic neurons was studied using combined fluorogold and immunocytochemical labeling. Four weeks after the 6-OHDA injection, there was an 85% reduction in the number of tyrosine hydroxylase (TH)-immunoreactive cells on the lesioned side. In contrast, there was only a 50% reduction in the number of fluorogold-labeled cells on the lesioned side. Second, the time course of the rescue of dopaminergic neurons after 6-OHDA by glial cell line-derived neurotrophic factor (GDNF) was determined using TH immunocytochemistry. Greater numbers of dopamine neurons were rescued 9 weeks after GDNF compared with counts made 5 weeks after GDNF. Taken together, these results suggest loss of dopaminergic phenotype is greater than cell loss following 6-OHDA injections, and that GDNF restores the phenotype of affected cells.