Find a Doctor or Practice Location

You can also search for providers and practices at Penn Medicine Lancaster General Health or Princeton Health.

I am searching for a
Reset Form
Dennis L. Kolson, MD, PhD

Dennis L. Kolson, MD, PhD Physician

Professor of Neurology Professor of Neurology Professor of Microbiology

Dr. Kolson is employed by Penn Medicine.

Patient Satisfaction Ratings

Patient Rating Breakdown

The Patient Satisfaction Rating is an average of all responses to the care provider related questions shown below from our nationally-recognized Press Ganey Patient Satisfaction Survey. Patients that are treated in outpatient or hospital environments may receive different surveys, and the volume of responses will vary by question.

Responses are measured on a scale of 1 to 5 with 5 being the best score.

Comments are submitted by patients and reflect their views and opinions. The comments are not endorsed by and do not necessarily reflect the views of Penn Medicine.

Overall Ratings

Clinical Specialties


  • Neurology

Programs & Centers:

Board Certification:

  • Neurology, 1990

Clinical Expertise:

  • Multiple Sclerosis (MS)

Practice Locations and Appointments

Insurance Accepted

  • Aetna US Healthcare
  • Cigna
  • Cigna HealthSpring
  • Clover Health Plan
  • CVS Health
  • Devon Health Services (Americare)
  • eLAP Services
  • Gateway Health Plan
  • Geisinger Health Plan
  • HealthAmerica / HealthAssurance, a Coventry Plan
  • HealthPartners
  • HealthPartners Medicare
  • HealthSmart
  • Highmark Blue Shield
  • Homestead Smart Health Plans
  • Horizon Blue Cross Blue Shield of New Jersey
  • Humana / Choicecare
  • Independence Blue Cross (Keystone East)
  • Intergroup
  • Keystone First
  • Keystone First Medicare
  • Multiplan
  • NJ Medicaid
  • NJ Qualcare
  • Oxford Health Plan
  • PA Health and Wellness (Centene) Medicare
  • PA Medicaid
  • PA Medicare
  • Preferred Health Care/LGH
  • Provider Partners Health Plan
  • Rail Road Medicare / Palmetto GBA
  • Remedy Partners at Penn Medicine
  • Tricare
  • United Healthcare
  • UnitedHealthcare Community Plan
  • US Family Health Plan
  • Veterans Choice Program

Education and Training

Medical School: University of Pittsburgh
Residency: Mercy Providence Hospital/UPMC Passavant Hospital
Residency: Duke University Medical Center
Fellowship: Hospital of the University of Pennsylvania


American Academy of Neurology, National American Association for the Advancement of Science, National American Society for Virology, National National NeuroAIDS Tissue Consortium/NIH Steering Committee, 2002-, National

Hospital Affiliation

Dr. Kolson is employed by Penn Medicine.

Hospital Privileges:

  • Hospital of the University of Pennsylvania: Has privileges to treat patients in the hospital.


Description of Research Expertise:

Research Interests
Mechansims and determinants of HIV induced neuronal injury. Neuronal cell responses to virus induced injury.

Key words: neuron, hippocampus, apoptosis, gene expression, single-cell mRNA, HIV, chemokine receptor, NMDA receptor.

Description of Research
My laboratory is focused upon pathogenesis of HIV-1-infection of the central nervous system (CNS) as a model for neuroimmune-mediated neurodegeneration. Within the CNS, HIV productively infects macrophages and microglia, with subsequent neuronal damage and loss by several mechanisms, including NMDA receptor mediated excitotoxicity and apoptosis. In vitro modeling shows that such infection results in the release of soluble neurotoxins that act in part through activation of neuronal NMDA receptors with subsequent activation of cell death pathways, including apoptosis cascades and calpain activation. Specific NMDA receptor subunits (NR2A, NR2B) are critical for such degeneration. In addition, dysregulation of glial (astrocyte, macrophage) neurotransmitter and oxidative functions may subserve both apoptotic and anti-apoptotic roles. HIV infection initiates neurodegeneration through mechanisms that are shared by other neurodegenerative diseases and understanding these mechanims has broad therapeutic implications for other such diseases.

Interestingly, neurons appear to initiate pro-survival resoponses to injury that involve release of neuropeptides and chemokines. We are focusing on one such unique neuropeptide, apelin, and its cognate receptor, APJ and the novel role that this receptor/ligand interaction might play in modulating neuronal responses to injury. We have found that apelin peptide is released by injury hippocampal and cortical neurons (in addition to physiological relase from pituicytes) and that it can modulate NMDA receptor function through phosphorylation, internalization, and suppression of NMDA receptors. We are thus focusing on how neuronal cell function is modulated by virally-induced stress responses in the CNS and how this applies to neurodegeneration, and how HIV infection might mimic other degenerative conditions. Major unanswered questions include:

1. What pathways are reponsible for neuronal damage and glial cell dysfunction in HIV infection?
2. How can NMDA receptor modulation alter neuronal susceptibility to HIV-induced damage?
3. Are specific genes turned on/off in neurons that are particularly vulnerable/resistant to HIV-induced injury?
4. What is the role of endogenous neuronal survival pathways (apelin/APJ) in preventing HIV-induced damage?
5. How can in vitro modeling be used to define targets for neuroprotection against HIV-1 and other neurodegenerative diseases?
6. How does the unfolded protein response (UPR) in HIV-infected macrophages modulate neurodegeneration?

To address these questions, we have developed several in vitro neuronal cell culture systems. We utilize primary rodent hippocampal and neocortical cell cultures as well as a unique human neuronal cell system utilizing NT2.N neurons in mixed neuronal/glial cell cultures to model HIV-1-induced neurodegeneration. We have developed a novel in vitro model using mixed cultures of human monocyte-derived macrophages with rodent neurons and astrocytes to analyze effects of HIV infection in the central nervous system. We have found that developmental susceptibility to HIV-1-induced neurodegeneration is determined by NMDA receptor subunit expression, and that the macrophage kynurenine metabolic pathway is a major contributor to the production of HIV-1-induced excitotoxin expression. We have also demonstrated that excitotoxic injury to neurons induces release of a novel neuropeptide, apelin, that can promote neuronal survival through modulation of NMDA receptors. Our current projects involve in vitro and in vivo analysis of cell death pathways in neurons that are induced by HIV-infected macrophages, analysis of the role of specific NMDA receptor subunits in determining neuronal vulnerability to HIV-induced damage, analysis of the unfolded protein response in macrophages and how it modulates neurodegeneration, and how apelin neuropeptide alters cellular responses through NMDA receptor modulation.

Rotation Projects
1. Analysis of NMDA receptor subunit expression and phosphorylation patterns in hippocampal and cortical neurons susceptible to HIV neurotoxicity

2. Analysis of the macrophage unfolded protein response.

3. Identification of the downstream pathways of death in neurons by HIV-1, including the role of calpain activation.

4. Analysis of apelin/APJ function in neural cells.

Lab personnel:
Patricia Vance, MS - Research Specialist
Lorraine Kolson, BS - Research Specialist
Denise Cook - Neuroscience PhD student
Stephanie Cross, Neuroscience MD/PhD student

Selected Publications:

Kolson DL, Sabnekar P, Baybis M and Crino PB: Gene expression in TUNEL-positive Neurons in HIV-infected brain J. Neurovirol. 10 ((suppl. 1)): 102-7,2004.

Patel SH, Kolson DL, Glosser G, Matozzo I, Ge Y, Babb JS, Mannon LJ and Grossman RI.: Correlation between percentage of brain parenchymal volume and neurocognitive performance in HIV infected patients. Am. J. Neuroradiol. 23 : 543-549,2002.

Chen W, Sulcove J, Frank I, Jaffer S, Ozdener H and Kolson DL.: Development of a human neuronal cell model for HIV/macrophage-induced neurotoxicity: apoptosis induced by HIV-1 primary isolates and evidence for involvement of the Bcl-2/Bcl-xL-sensitive intrinsic apoptosis pathway. J. Virology 76 : 9407-9419,2002.

Ge Y, Grossman RI, Babb JS, Rabin ML, Mannon LJ and Kolson DL.: Age-related total gray matter and white matter changes in normal adult brain. Part I. Volumetric MR imaging analysis. Am. J. Neuroradiol. 23 : 1327-1333,2002.

Ge Y, Grossman RI, Babb JS, Rabin ML, Mannon LJ and Kolson DL.: Age-related total gray matter and white matter changes in normal adult brain. Part II: quantitative magnetization transfer ratio histogram analysis. Am. J. Neuroradiol. 23 : 1334-1341,2002.

O’Donnell, LA, Chen W, Agrawal A, Sulcove J and Kolson DL.: Potential neuroprotective role of APJ/apelin interactions: protection against HIV-induced apoptosis. NIMH workshop: Viral and Host Genetic Factyors Regulating HIV/CNS Disease, Rockville, MD. : 2002.

Martin-Garcia J, Kolson DL, Gonzalez-Scarano F.: Chemokine receptors in the brain: their role in HIV infection and pathogenesis. AIDS (in press). : 2002.

Kolson DL.: Neuropathogenesis of central nervous system HIV-1 infection. Clin. Lab. Med. 22 : 1-15,2002.

Ge Y, Grossman RL, Udupa JK, Babb JS, Kolson DL and McGowan JC.: Magnetization transfer ratio histogram analysis of gray matter in relapsing-remitting multiple sclerosis. Am. J. Neuroradiol. 22 : 470-475,2001.

Ge Y, Grossman RL, Udupa JK, Babb JS, Nyul LG and Kolson DL.: Brain atrophy in relapsing-remitting multiple sclerosis: fractional volumetric analysis of gray matter and white matter. Radiology 220 : 606-610,2001.

View all publications

Academic Contact Info

280C Clinical Research Building
University of Pennsylvania
415 Curie Blvd.

Philadelphia, PA 19104/6146
Phone: (215) 573-3505
Patient appointments: 800-789-7366 (PENN)

Related Links