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| First Name: | Brian | | Last Name: | Balin | | Title: | Professor | | Advanced Degrees: | PhD | | Affiliation: | Philadelphia College of Osteopathic Medicine | | Department: | Pathology/Microbiology & Immunology | | Street Address 1: | 4170 City Avenue | | Street Address 2: | 3rd floor, Evans Hall | | City: | Philadelphia | | State/Province: | PA | | Zip/Postal Code: | 19131 | Country/Territory: | U.S.A. | | Phone: | 215-871-6862 | | Fax: | 215-871-6869 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 8 June 2003]
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View all comments by Brian Balin
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Parkinson Disease, Polyglutamine Disorders (Huntington's, etc.), Prion Diseases, Stroke and Trauma, Alzheimer Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Tauopathies, Aging Process
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Oxidative Stress, DNA microarrays, Proteomics, Microscopy, Molecular and Cell biology, Apoptosis/Cell cycle, Neurobiology, Neuroimmunology, Neuropathology, Protein structure/chemistry, Signal transduction, Neuro-infection & neuro-inflammation, A-beta PP/A-beta, Animal Models, Tau/Cytoskeleton
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ACADEMIC CREDENTIALS:
1980-1987, Ph.D. - Experimental Pathology; Major Discipline: Exp. Neuropathology: University of Maryland School of Medicine at Baltimore; Balto., Md.
1976-1977, Post-Baccalaureate - Microbiology - University of Maryland, College Park, Md.
1972-1976, B.S. - Microbiology - University of Maryland, College Park, Md.
PROFESSIONAL APPOINTMENTS:
Professor (1999-present) - Department of Pathology, Microbiology and Immunology
Philadelphia College of Osteopathic Medicine, Philadelphia, PA
Associate Professor (1998-1999) - Department of Pathology, Microbiology and Immunology
Philadelphia College of Osteopathic Medicine, Philadelphia, PA
Associate Professor (1995-1998) - Department of Pathology and Laboratory Medicine
Allegheny University of the Health Sciences, Philadelphia, PA.
Assistant Professor (1990-1995) - Department of Pathology and Laboratory Medicine
Medical College of Pennsylvania & Hahnemann University, Philadelphia, PA
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Balin, B.J., Broadwell, R.D., Salcman, M. and El-Kalliny, M.: Avenues for entry of peripherally administered protein to the central nervous system in mouse, rat and squirrel monkey. J. Comp. Neurol. 251(2): 260-280, 1986.
Lee, V.M.-Y., Balin, B.J., Otvos Jr., L., Hollosi, M. and Trojanowski, J.Q.: A68: A major subunit of paired helical filaments and derivatized forms of normal Tau. Science 251: 675-678, 1991.
Appelt, D.M. and Balin, B.J.: Analysis of paired helical filaments found in Alzheimer's Disease using freeze-drying/rotary shadowing. J. Struct. Biol. 111: 85-95,1993.
Appelt, D.M., Kopen, G.C., Boyne, L.J. and Balin, B.J.: Localization of transglutaminase in hippocampal neurons: Implications for Alzheimer Disease. J. Histochem. Cytochem. 44: 1421-1427, 1996.
Appelt, D.M. and Balin, B.J.: The association of tissue transglutaminase with human recombinant tau results in the formation of insoluble filamentous structures. Brain Res. 745:21-31, 1997.
Balin, B.J., Gérard, H.C., Arking, E.J., Appelt, D.M., Branigan, P.J., Abrams, J.T., Whittum-Hudson, J.A., and Hudson, A.P.: Identification and localization of Chlamydia pneumoniae in the Alzheimer's brain. Med. Micro. & Immunol. 187:23-42, 1998.
Arking, E.J., Appelt, D.M., Kolby, S.J., Abrams, J.T., and Balin, B.J.: Ultrastructural Analysis of Chlamydia pneumoniae in the Alzheimer's brain. Pathogenesis 1(3):210-211, 1999.
MacIntyre, A., Hammond, C.J., Little, C.S., Appelt, D.M., Balin, B.J.: Chlamydia pneumoniae infection alters the junctional complex proteins of human brain microvascular endothelial cells. FEMS Microbiology Letters 217: 167-172, 2002.
MacIntyre, A., Abramov, R., Hammond, C.J., Little, C.S., Appelt, D.M., Balin, B.J.: Chlamydia pneumoniae infection of human brain endothelial cells and monocytes promotes the transmigration of monocytes through an in vitro blood brain barrier. J. Neurosci. Res. 71: 740-750, 2003.
Little, C.S., Hammond, C.J., MacIntyre, A., Balin, B.J. , Appelt, D.M. : Induction of Alzheimer's disease-like pathology in the brains of young, non-transgenic, Balb/c mice following infection with Chlamydia pneumoniae: A model for late-onset sporadic Alzheimer's Disease. (in press, Neurobiol. of Aging), 2003.
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1. Understanding causal agents in the induction of late-onset sporadic Alzheimer's disease.
2. Linkage of neuro-infection as a primary inducer of neuroinflammation.
3. Unifying factors that help to explain how all the major pathologies correlate with one another. |
1. Animal models studying how infection/inducers of inflammation trigger events important to the pathogenesis of AD.
2. Clinical trials based on infectious modalities as principal agents in the pathogenesis of AD.
3. Intensive screening of archival tissues with state of the art molecular, cell biological, and ultrastructural techniques specifically looking for evidence of infectious agents correlating to AD pathology. |
We believe that infection with the respiratory pathogen Chlamydia pneumoniae is a causative agent in sporadic Alzheimer's disease. In addition, other infectious agents may contribute in a polymicrobial manner to stimulate neuroinflammatory responses resulting in AD pathology. |
Currently, we have developed an animal model based on infection in which the generation of amyloid plaques occur in the normal mouse brain following Intranasal delivery of Chlamydia pneumoniae. We believe that with extended periods of time following infection, and possibly with re-infection, that neurofibrillary pathology will develop in the mouse brains. If this occurs, then we will have provided "Proof of Principle" that Chlamydia pneumoniae infection is responsible for the ultimate generation of the major AD pathological entities. This would be the closest that anyone has come to determining that infection can cause AD! |
As a scientific community, we are still fairly infantile in our understanding of chronic infections as they relate to chronic diseases throughout the body. Lessons have been learned continually that diseases such as cancer, ulcers, cardiovascular disease, etc. that typically are not thought of as INFECTIOUS, actually have significant infectious components! Our fallback position is that infection can be both a primary and secondary factor in many disease processes. The importance of infection can not be minimized even if it is SECONDARY or opportunistic. Often a person succumbing to a disease process, succumbs due to a secondary issue. One example, is HIV and AIDS, in which secondary infections with agents such as cytomegalo virus, pneumocystis carinii, toxoplasma, etc often will result in exacerbated morbidity and/or mortality!!
Thus, our position is that infection of any sort associated with neurodegenerative conditions should not be and can not be dismissed or ignored. We can not reduce the problem to only a small subset of issues. Infection must be considered as a major environmental influence in our major neurodegenerative conditions, along with other environmental insults, and with an understanding of genetic susceptibility factors. |
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