Daniel A. Peterson

ORCID: 0000-0001-7275-6403
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About
Contact & Profiles
Research Areas
  • Neurogenesis and neuroplasticity mechanisms
  • Nerve injury and regeneration
  • Axon Guidance and Neuronal Signaling
  • Alzheimer's disease research and treatments
  • Pluripotent Stem Cells Research
  • Lysosomal Storage Disorders Research
  • Innovative Microfluidic and Catalytic Techniques Innovation
  • Point processes and geometric inequalities
  • Neuroscience and Neuropharmacology Research
  • Cell Image Analysis Techniques
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Virus-based gene therapy research
  • MicroRNA in disease regulation
  • Mesenchymal stem cell research
  • Calcium signaling and nucleotide metabolism
  • Electrohydrodynamics and Fluid Dynamics
  • RNA Interference and Gene Delivery
  • Gold and Silver Nanoparticles Synthesis and Applications
  • Anesthesia and Neurotoxicity Research
  • Advanced Fluorescence Microscopy Techniques
  • Molecular Biology Techniques and Applications
  • Traumatic Brain Injury Research
  • Genetics and Neurodevelopmental Disorders
  • Microfluidic and Bio-sensing Technologies
  • Traumatic Brain Injury and Neurovascular Disturbances

Rosalind Franklin University of Medicine and Science
2012-2024

Life & Brain (Germany)
2015

University of Bonn
2015

Oregon State University
2011-2014

Franklin University
2002-2014

Breakthrough Institute
2014

University of Massachusetts Chan Medical School
2014

Salk Institute for Biological Studies
1995-1999

Torrey Pines Institute For Molecular Studies
1997

Whittier College
1994

The dentate gyrus of the hippocampus is one few areas adult brain that undergoes neurogenesis. In present study, cells capable proliferation and neurogenesis were isolated cultured from rat hippocampus. defined medium containing basic fibroblast growth factor (FGF-2), can survive, proliferate, express neuronal glial markers. Cells have been maintained in culture for 1 year through multiple passages. These labeled vitro with bromodeoxyuridine adenovirus expressing beta-galactosidase...

10.1073/pnas.92.25.11879 article EN public-domain Proceedings of the National Academy of Sciences 1995-12-05

Abstract: 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) reduction is one of the most frequently used methods for measuring cell proliferation and neural cytotoxicity. It widely assumed that MTT reduced by active mitochondria in living cells. By using isolated from rat brain B12 cells, we indeed found malate, glutamate, succinate support mitochondria. However, data presented this study do not exclusive role intact Using a variety approaches, cells confined to...

10.1046/j.1471-4159.1997.69020581.x article EN Journal of Neurochemistry 1997-08-01

Primary embryonic hippocampal neurons can develop morphologically and functionally in culture but do not survive more than a few weeks. It has been reported that basic fibroblast growth factor (bFGF) promotes the survival of neurite elongation from fetal neurons. We report bFGF, dose-dependent manner, induce (50 pg to 1 ng/ml) proliferation (10-20 progenitor vitro. In serum-free medium containing high concentrations only proliferated (4-day doubling time) differentiated also could be...

10.1073/pnas.90.8.3602 article EN Proceedings of the National Academy of Sciences 1993-04-15

A neuropathological hallmark of Alzheimer's disease is the deposition amyloid-beta (Abeta) peptides in senile plaques hippocampus and cerebral cortex. Abeta derived from larger integral membrane proteins termed amyloid precursor (APP). We demonstrated previously that APP, synthesized by neurons entorhinal cortex, transported via perforant pathway to presynaptic terminals dentate gyrus. reported that, although full-length APP membrane-tethered, C-terminal derivatives (APP-CTFs) accumulate at...

10.1523/jneurosci.22-22-09785.2002 article EN Journal of Neuroscience 2002-11-15

Factors modulating neurogenesis may contribute to the pathophysiology of affective disorders such as major depression. Environmental stressors in animal models have been proposed alter neurogenesis, suggesting a mechanism for this contribution. The effect an acute psychosocial stressor on either proliferation or survival (immediate, short term, and long term) was examined along with subsequent neuronal differentiation hippocampus adult male Sprague Dawley rats. Subjects were exposed widely...

10.1523/jneurosci.3849-06.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-03-14

Late infantile neuronal ceroid lipofuscinosis (LINCL) is a lysosomal storage disorder caused by mutations in the CLN2 gene and deficiency of tripeptidyl peptidase I (TPP-I). Prior studies with adeno-associated virus (AAV) serotype 2 or 5 mediated transfer complementary DNA to central nervous system (CNS) CLN2−/− mice cleared CNS granules, but provided no improvement phenotype survival this model LINCL. In study, AAV serotypes (AAV2, AAV5, AAV8, AAVrh.10) were compared for delivery same...

10.1038/sj.mt.6300049 article EN cc-by-nc-nd Molecular Therapy 2006-12-19

Abstract Mesenchymal stem cells (MSCs) have been investigated as a clinical therapy to promote tissue repair. However, the disappearance of grafted soon after engraftment suggests possible role initiators repair rather than effectors. We evaluated relative contribution human MSCs and host stem/progenitor in promoting wound healing by using novel asymmetric model normal impaired diabetic (db/db) mice discriminate between effect direct subsequent systemic response. Experimental animals...

10.5966/sctm.2012-0041 article EN cc-by-nc Stem Cells Translational Medicine 2012-12-21

The cellular heterogeneity and complex circuitry of the central nervous system make it difficult to achieve precise delivery experimental therapeutic agents. We report here an in vivo retrograde gene strategy target mature projection neurons using adeno-associated virus, a vector with low toxicity capacity for long-term expression. Viral axon terminal fields hippocampus striatum resulted viral internalization, transport, transgene expression specific entorhinal cortex substantia nigra....

10.1006/mthe.2001.0520 article EN cc-by-nc-nd Molecular Therapy 2002-01-01

Abstract Substantial dysfunction and loss of cholinergic neurons occur in Alzheimer's disease (AD). Nerve growth factor (NGF) is a potent neurotrophic for basal forebrain neurons, the use NGF to stimulate residual dysfunctional cells AD being considered. To define effects on other cell populations brain, was continuously infused into lateral ventricle rats 7 weeks. At end treatment, Schwann hyperplasia abundant sensory sympathetic neurite sprouting were observed subpial region medulla...

10.1002/ana.410410114 article EN Annals of Neurology 1997-01-01

Abstract Endogenous stem cells in the bone marrow respond to environmental cues and contribute tissue maintenance repair. In type 2 diabetes, a multifaceted metabolic disease characterized by insulin resistance hyperglycemia, major complications are seen multiple organ systems. To evaluate effects of this on endogenous cell population, we used diabetic mouse model (db/db), which recapitulates these phenotypes. Bone marrow-derived mesenchymal (MSCs) from db/db mice were vitro using flow...

10.5966/sctm.2012-0031 article EN cc-by-nc Stem Cells Translational Medicine 2012-01-26

Astrocytes secrete growth factors that are both neuroprotective and supportive for the local environment. Identified by glial fibrillary acidic protein (GFAP) expression, astrocytes exhibit heterogeneity in morphology expression of phenotypic markers throughout different adult brain regions. In neurogenic niches, vascular endothelial factor (VEGF) fibroblast factor-2 (FGF-2) within niche also a source special GFAP-positive multipotent neural stem cells (NSCs). Normal aging is accompanied...

10.1111/j.1474-9726.2011.00694.x article EN other-oa Aging Cell 2011-03-08

Identifying effective strategies to prevent memory loss in AD has eluded researchers date, and likely reflects insufficient understanding of early pathogenic mechanisms directly affecting encoding. As synaptic best correlates with AD, refocusing efforts identify factors driving impairments may provide the critical insight needed advance field. In this study, we reveal a previously undescribed cascade events underlying pre postsynaptic hippocampal signaling deficits linked cognitive decline...

10.1186/s13024-019-0307-7 article EN cc-by Molecular Neurodegeneration 2019-01-22

Impairments in neural lysosomal- and autophagic-mediated degradation of cellular debris contribute to neuritic dystrophy synaptic loss. While these are well-characterized features neurodegenerative disorders such as Alzheimer's disease (AD), the upstream processes driving deficits pathogenic protein mishandling less understood. Using a series fluorescent biosensors optical imaging model cells, AD mouse models human neurons derived from patients, we reveal previously undescribed signaling...

10.1073/pnas.2211999119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-11-28

Amyloid β peptide (Aβ) is thought to play a central role in the pathogenesis of Alzheimer disease (AD). How Aβ induces neurodegeneration AD not known. A connection between and cholesterol metabolism suggested by finding that people with apolipoprotein E4 allele, locus coding for cholesterol-transporting lipoprotein, have modified risk both late-onset cardiovascular disease. In present study we show submicromolar concentrations free alter trafficking population intracellular vesicles are...

10.1073/pnas.95.22.13266 article EN Proceedings of the National Academy of Sciences 1998-10-27

Abstract The goal of this study was to understand how dopamine receptors, which are activated during psychostimulant administration, might influence glutamate‐dependent forms synaptic plasticity that increasingly recognized as important drug addiction. Regulation the surface expression α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptor subunit GluR1 plays a critical role in long‐term potentiation, well‐characterized form plasticity. Primary cultures rat nucleus accumbens...

10.1046/j.1471-4159.2002.01164.x article EN Journal of Neurochemistry 2002-10-17
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