|
|
|
|
|
| First Name: | Michael | | Last Name: | D'Andrea | | Title: | Chief Scientist | | Advanced Degrees: | Ph.D., M.S. | | Affiliation: | Slidomics, LLC | | Street Address 1: | 14 Anders Drive | | City: | Cherry Hill | | State/Province: | NJ | | Zip/Postal Code: | 08003 | Country/Territory: | U.S.A. | | Phone: | 609-230-6872 | | Email Address: |  |
Disclosure:
(view policy)
|
|
|
|
View all comments by Michael D'Andrea
|
Alzheimer Disease, Stroke and Trauma, Parkinson Disease, Aging Process, Neuromuscular Disorders (ALS, etc.)
|
Molecular and Cell biology, Neuropathology, Apoptosis/Cell cycle, Neurobiology, Neuroimmunology, Proteomics, Bioinformatics/Statistics, Microscopy, A-beta PP/A-beta
|
Mechanisms of cell death and amyloid plaque formation in AD and how they relate to normal aging processes. |
1.D’Andrea MR, Nagele RG. Morphologically distinct types of amyloid plaques point the way to a better understanding of Alzheimer’s disease pathogenesis. Biotechnic and Histochemistry, in press, 2009
2.D’Andrea MR, Nagele R, Lee DHS, Wang H-Y. Targeting intracellular Ab for Alzheimer’s disease drug discovery. Drug Development Research, 51:1-7, 2002.
3.D’Andrea MR, Nagele RG. MAP-2 immunolabeling can distinguish diffuse from dense-core amyloid plaques in Alzheimer’s disease brains. Biotechic & Histochemistry, 77(2):95-103, 2002.
4.D’Andrea MR, Nagele RG, Gumula NA, Reiser PA, Polkovitch DA, Hertzog BM, Andrade-Gordon P. Lipofuscin and Ab42 exhibit distinct distribution patterns in normal and Alzheimer’s disease brains. Neuroscience Letters, 323(1):45-49, 2002.
5.Wang H-Y, D’Andrea MR, Nagele RG. Cerebellar diffuse amyloid plaques are derived from dendritic Ab42 accumulations in Purkinje cells. Neurobiology of Aging, 23(2):213-223, 2002.
6.Nagele RG, D’Andrea MR, Wang H-Y. Intraneuronal accumulation of b-amyloid 1-42 is mediated by the a7 nicotinic acetylcholine receptor in Alzheimer’s disease. Neuroscience, 110(2):199-211, 2002.
7.D'Andrea MR, Ilyin S, Plata-Salaman CR. Abnormal patterns of microtubule-associated protein-2 (MAP-2) immunolabeling in neuronal nuclei and Lewy bodies in Parkinson’s disease substantia nigra brain tissues. Neuroscience Letters, 306 (3):137-140, 2001.
8.D’Andrea MR, Reiser PA, Gumula NA, Hertzog BM, Andrade-Gordon P. Application of triple-label immunohistochemistry to characterize inflammation in Alzheimer’s disease brains. Biotechnic & Histochemistry 76 (2), 97-106, 2001 (cover photograph).
9.Wang H-Y, D’Andrea MR, Drouillard A-M S, Plata-Salaman CR, Shank RP, Reitz AB, Lee DHS. Differential affinities for the a7 nicotinic acetylcholine receptors distinguish b-amyloid 1-40 from b-amyloid 1-42. J Pharmacol & Exp Therap, in press, 2001.
10.D’Andrea MR, Nagele RG, Wang H-Y, Peterson PA, Lee DHS. Evidence that neurons accumulating amyloid can undergo lysis to form amyloid plaques in Alzheimer’s disease. Histopathology, 38 (2), 120-134, 2001.
|
The basics! Amyloid plaque formation, cell death. etc. |
have to get back to you on this...I read many to find the 'top' 3, |
1) plaques form from various mechanisms, some of which do NOT have pathological consequences;
2) field currently confuses this basic concept and has touble correlation plaques (generally applied term) to clinical symptology;
3) field very confused on terms of plaques and a nomenclaure is needed....dense-core = neuritic = senile not vascular, diffuse, etc.
4) some plaques (dense-core) have pathological consequences such as the death of the cell and hence inflammation;
5) inflammation brings in secondary cell death and apoptosis......etc. |
1) objectivity, remove 'pet' hypothesis (although I fully respect all hypothesis), or at least consider 'other' possibilities...reviewers can be very 'protective' for obvious reasons;
2) since no in vivo models exist in human...many go to in vitro and animal model, all of which need to be assessed in their proper context;
3) clinical data is not tight to determine true onset etc.
4) unfortunately, there are many limitations or missing pieces of evidence in the human condition. |
I look at human tissues only....one can say that my interpretations are based on 'static ' images, but so are those in the sky, yet we hypothesize about the expanding universe...controls tissues are on the continuum to AD, but something (of which I do not know) dramatically separates the controls from AD. |
|
|
|
|
|
|
Home
