Dr. Frosch

	Department of Pathology
	Brigham and Women's Hospital
	A teaching Affliate of Harvard Medical School
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Name and Present Position:

MATTHEW P. FROSCH, Consultant Neuropathologist

Address:

C.S. Kubik Laboratory for Neuropathology, Department of Pathology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114

Medical School (including school name, date and degree awarded):

1987 MD, Harvard Medical School, Boston, MA
1987 PhD (Biophysics), Harvard University, Cambridge, MA

Graduate Medical Education (including dates and institution of internships, residencies, fellowships, etc.):

1987-89 Resident in Anatomic Pathology, Brigham and Women's Hospital
1989 Chief Resident in Anatomic Pathology and Senior Resident in Surgical Pathology, Brigham and Women's Hospital
1990-92 Resident in Neuropathology, Joint Training Program, Brigham and Women's and Children's Hospitals, Boston, MA

Certification:

1988 National Board of Medical Examiners
1992 American Board of Pathology (Neuropathology and Anatomic Pathology)

Current Academic Appointment(s):

Associate Professor of Pathology, Harvard Medical School

Current Medical Staff Appointments:

Consultant Neuropathologist, Brigham and Women's Hospital
Director, Neuropathology Service, Massachusetts General Hospital, Boston, MA

Selected Bibliography:

Domnitz SB, Robbins EM, Hoang AW, Garcia-Alloza M, Hyman BT, Rebeck GW, Greenberg SM, Bacskai BJ, Frosch MP. Progression of CAA in Transgenic Mouse Models of AD. J Neuropathol Exp Neurol. 2005, 64:588-94.
Robbins EM, Betensky RA, Domnitz SB, Purcell SM, Garcia-Alloza M, Greenberg C, Rebeck GW, Hyman BT, Greenberg SM, Frosch MP, Bacskai BJ. Kinetics of Cerebral Amyloid Angiopathy progression in a transgenic mouse model of Alzheimer disease. J Neurosci. 2006, 26:365-371.
Garcia-Alloza M, Robbins EM, Zhang-Nunes SX, Purcell SM, Betensky RA, Raju S, Prada C, Greenberg SM, Bacskai BJ, Frosch MP. Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease. Neurobiol Dis. 2006. 24:516-24.
Zhang-Nunes SX, Maat-Schieman MLC, van Duinen SG, Roos RAC, Frosch MP, Greenberg SM. The Cerebral â-Amyloid Angiopathies: Hereditary and Sporadic. Brain Pathol. 2006. 16:30-9.
Prada C, Garcia-Alloza M, Zhang-Nunes SX, Betensky RA, Greenberg SM, Bacskai BJ, Frosch MP. Antibody-mediated clearance of Aâ from Cerebral Amyloid Angiopathy revealed by quantitative in vivo imaging. J. Neurosci. 2007, 27:1973-80.
Bacskai BJ, Frosch MP, Freeman SH, Raymond SB, Augustinack JC, Johnson KA, Irizarry MC, Klunk WE, Mathis CA, DeKosky ST, Greenberg SM, Hyman BT, Growdon JH. Molecular Imaging With Pittsburgh Compound B Confirmed at Autopsy: A Case Report. Arch Neurol. 2007; 64:431-434.
Freeman SH, Raju S, Hyman BT, Frosch MP, Irizarry MC. Plasma Aâ levels do not reflect brain Aâ levels. J. Neuropathol Exp Neurol. 2007, 66:264-271.
Simon DK, Rodriguez ML, Frosch MP, Quackenbush EJ, Fekse SK, Natowicz MR. A unique familial leukodystrophy with adult onset dementia and abnormal glycolipid storage: a new lysosomal disease? J Neurol Neurosurg Psychiat 1998; 65:251-254.
Soriano SG, Coxon A, Wang YF, Frosch MP, Lipton SA, Hickey, PR, Mayadas TN. Mice deficient in Mac-1 [CD11b/CD18] are less susceptible to cerebral ischemia reperfusion injury, Stroke, 1999; 30:134-139.
Berezovska O. McLean P, Knowles R, Frosch, MP, Lu SM, Lux SE, Hyman B. Notch1 inhibits neurite outgrowth in postmitotic primary neurons. Neuroscience, 1999; 93:433-439.
Albarracin CT, Frosch MP, Chin WW. The gonadotrophin-releasing hormone receptor gene promoter directs pituitary-specific oncogene expression in transgenic mice. Endocrinology, 1999; 140:2415-2421.
Berezovska O, Frosch MP, McLean P, Knowles R, Koo E, Kang D, Lu FM, Lux SE, Shen OJ, Tonegawa S, Human BT. Presenilin 1 facilitates Notch 1 effect on neurite outgrowth in primary mammalian neurons. Molec Brain Res, 1999; 69:273-280.

Kang DE, Soriano S, Frosch MP, Collins T, Naruse S, Sisodia SS, Koo EH. Presenilin 1 alters the processing of ß-catenin: evidence for dominant negative activity of Alzheimer's disease linked mutations on ß-catenin half-life. J Neurosci, 1999; 19:4229-4237.