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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:precious
Last Name:agbonkpolor
Title:doctor
Advanced Degrees:advance degree in Epidemiology
Affiliation:pears technological global co-operation
Department:human research and clinical medicine
Street Address 1:59 eweka road upper siloko road egor quater's
Street Address 2:59 eweka road upper siloko road egor quater's
City:benin city edo state nigeria
State/Province:edo state
Zip/Postal Code:23452
Country/Territory:Nigeria
Phone:08030649498
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 15 September 2010]
Clinical Interests:
Neurodevelopmental Disorders (Down syndrome, etc.), Alzheimer Disease, Stroke and Trauma, Neuromuscular Disorders (ALS, etc.), Parkinson Disease
Research Focus:
Diagnosis, Protein structure/chemistry, Molecular and Cell biology, Bioinformatics/Statistics, Neuroimmunology, Neurotransmission, Electrophysiology, Oxidative Stress, DNA microarrays, Proteomics, Neuropathology, Clinical trials, Drug screening, Chemistry/Pharmacology, Signal transduction, Stem cells, Epidemiology, Microscopy, Neurobiology, Genetics
Work Sector(s):
Research institute, Medical hospital, University
Web Sites:
Personal: no
Professional: no
Lab: no
Researcher Bio
next time
Top Papers
nil
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Lack of an awareness of the Cystic, cell wall
deficient.
Lack of an appreciation of Spirochete to Human
transfection, as a mechanism for production of
varoius mutations in the Human genome.
Lack of awareness of the models of intraneuronal
(intracellular) infections for various neurotropic agents as a conceptual model to understand the ontogeny of Neurofibrillary tangles.
Lack of the awareness of infections which cross synapses- in the model of Pseudorabies- to serve as a potential explanation for the
progressions of Alzheimer's disease.
Neurodegenerative diseases are characterized by a number of features including the protein clumps called inclusions; decline of nerve-cell synapses; and the selective loss of the nerve cells themselves.

What are the top three papers (not yours) you have read recently?
1: Stem cells and neurodegenerative disease: cool science and scepticism by Monya Baker.

2:Suppression of basal autophagy in neural cells
causes neurodegenerative disease in mice by T Hara, K Nakamura, M Matsui, A Yamamoto

3:A transmembrane form of the prion protein in neurodegenerative disease by RS Hegde, JA Mastrianni, MR Scott, KA DeFea

4:Filamentous nerve cell inclusions in neurodegenerative diseases by M Goedert, MG Spillantini, SW Davies - Current Opinion in Neurobiology.
If resources were not limited, what research projects would you pursue?
Neurodegenerative Diseases.
Neurodegenerative Disorders.
Molecular Neurodegeneration.
What is your leading hypothesis?
Common cellular and molecular mechanisms underlie different neurodegenerative diseases, from Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis to sporadic prion diseases. The molecular mechanisms include aberrant protein folding and aggregation in the form of extracellular plaques or intracellular inclusions.
Deeper understanding of the detailed mechanism of protein aggregation and cellular toxicity should lead to rational drug design for this type of disease. Our studies of human stefin B, a model amyloidogenic protein, need to be reviewed. The studies range from establishing the mechanism, imaging the fibrillar and prefibrillar species by transmission electron microscopy (TEM) and atomic force microscopy (AFM), to structural studies of the precursor oligomeric states.


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