Mark Stuart Forman, MD, Duke University 1995, PhD, Rockefeller University 1994
Affiliations: | Experimental Medicine | Merck Pharmaceuticals, Lincoln, NJ, United States |
Area:
Molecular pathogeneis of neurodegenerative diseaseWebsite:
http://www.med.upenn.edu/cndr/MarkFormanbio.shtmlGoogle:
"Mark Forman"Bio:
http://www.healthgrades.com/directory_search/physician/profiles/dr-md-reports/dr-mark-forman-md-63abc066/hospital-affiliations
EXPERIMENTAL MEDICINE UG4D 034
PO BOX 1000
NORTH WALES, PA 194541099
United States
Mean distance: 14.88 (cluster 24) | S | N | B | C | P |
Cross-listing: Neurotree - Neuropathology Tree
Parents
Sign in to add mentor| Jeffrey A. Golden | post-doc | Children’s Hospital of Philadelphia / University of Pennsylvania (Neurotree) | ||
| Nicholas K. Gonatas | post-doc | Penn (Neurotree) | ||
| (Late 1990's) | ||||
| Virginia Man-Yee Lee | post-doc | Penn (Neurotree) | ||
| (Late 1990's) | ||||
| John Q. Trojanowski | post-doc | Penn (Neurotree) | ||
| (Late 1990's) | ||||
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Publications
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| Rabinovici GD, Carrillo MC, Forman M, et al. (2017) Multiple comorbid neuropathologies in the setting of Alzheimer's disease neuropathology and implications for drug development. Alzheimer's & Dementia (New York, N. Y.). 3: 83-91 |
| Scott JD, Li SW, Brunskill AP, et al. (2016) Discovery of the 3-Imino-1,2,4-thiadiazinane 1,1-Dioxide Derivative Verubecestat (MK-8931)-A β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Inhibitor for the Treatment of Alzheimer's Disease. Journal of Medicinal Chemistry. 59: 10435-10450 |
| Hu WT, McMillan C, Libon D, et al. (2010) Multimodal predictors for Alzheimer disease in nonfluent primary progressive aphasia. Neurology. 75: 595-602 |
| Ritson GP, Custer SK, Freibaum BD, et al. (2010) TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 30: 7729-39 |
| Gitcho MA, Strider J, Carter D, et al. (2009) VCP mutations causing frontotemporal lobar degeneration disrupt localization of TDP-43 and induce cell death. The Journal of Biological Chemistry. 284: 12384-98 |
| Neumann M, Kwong LK, Lee EB, et al. (2009) Phosphorylation of S409/410 of TDP-43 is a consistent feature in all sporadic and familial forms of TDP-43 proteinopathies. Acta Neuropathologica. 117: 137-49 |
| Weihl CC, Temiz P, Miller SE, et al. (2008) TDP-43 accumulation in inclusion body myopathy muscle suggests a common pathogenic mechanism with frontotemporal dementia. Journal of Neurology, Neurosurgery, and Psychiatry. 79: 1186-9 |
| Uryu K, Nakashima-Yasuda H, Forman MS, et al. (2008) Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies. Journal of Neuropathology and Experimental Neurology. 67: 555-64 |
| Bian H, Van Swieten JC, Leight S, et al. (2008) CSF biomarkers in frontotemporal lobar degeneration with known pathology. Neurology. 70: 1827-35 |
| Grossman M, Xie SX, Libon DJ, et al. (2008) Longitudinal decline in autopsy-defined frontotemporal lobar degeneration. Neurology. 70: 2036-45 |