Targeted Intraparenchymal Delivery of Human NGF by Gene Transfer to the Primate Basal Forebrain for 3 Months Does Not Accelerate β-Amyloid Plaque Deposition

1998 ◽  
Vol 154 (2) ◽  
pp. 573-582 ◽  
Author(s):  
Mark H. Tuszynski ◽  
David E. Smith ◽  
Jeffrey Roberts ◽  
Heather McKay ◽  
Elliott Mufson
Keyword(s):  
Gene Transfer ◽  
Basal Forebrain ◽  
Amyloid Plaque ◽  
Plaque Deposition ◽  
Β Amyloid

scholarly journals Tau deletion impairs intracellular β-amyloid-42 clearance and leads to more extracellular plaque deposition in gene transfer models

2014 ◽  
Vol 9 (1) ◽  
pp. 46 ◽  
Author(s):  
Irina Lonskaya ◽  
Michaeline Hebron ◽  
Wenqiang Chen ◽  
Joel Schachter ◽  
Charbel Moussa
Keyword(s):  
Gene Transfer ◽  
Plaque Deposition ◽  
Β Amyloid ◽  
Transfer Models

scholarly journals PET/SPECT imaging agents for neurodegenerative diseases

2014 ◽  
Vol 43 (19) ◽  
pp. 6683-6691 ◽  
Author(s):  
Lin Zhu ◽  
Karl Ploessl ◽  
Hank F. Kung
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Neurodegenerative Diseases ◽  
Pet Imaging ◽  
Amyloid Plaque ◽  
Spect Imaging ◽  
Imaging Agents ◽  
Plaque Deposition ◽  
Β Amyloid

Amyvid/PET imaging of a living brain detects β-amyloid plaque deposition, a risk factor for developing Alzheimer's disease.

Novel imaging agents for β-amyloid plaque based on the N-benzoylindole core

2011 ◽  
Vol 21 (18) ◽  
pp. 5594-5597 ◽  
Author(s):  
Yang Yang ◽  
Xin-Hong Duan ◽  
Jun-Yuan Deng ◽  
Bing Jin ◽  
Hong-Mei Jia ◽  
...  
Keyword(s):  
Amyloid Plaque ◽  
Imaging Agents ◽  
Β Amyloid

Laser microdissection reveals regional and cellular differences in GFAP mRNA upregulation following brain injury, axonal denervation, and amyloid plaque deposition

Glia ◽  
2004 ◽  
Vol 48 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Guido J. Burbach ◽  
Doris Dehn ◽  
Domenico Del Turco ◽  
Matthias Staufenbiel ◽  
Thomas Deller
Keyword(s):  
Brain Injury ◽  
Laser Microdissection ◽  
Amyloid Plaque ◽  
Plaque Deposition

scholarly journals New Biochemical Insights to Unravel the Pathogenesis of Alzheimer's Lesions

1991 ◽  
Vol 18 (S3) ◽  
pp. 408-410 ◽  
Author(s):  
Alex E. Roher ◽  
Kenneth C. Palmer ◽  
John Capodilupo ◽  
Arun R. Wakade ◽  
Melvyn J. Ball
Keyword(s):  
Amyloid Plaque ◽  
Extracellular Proteins ◽  
High Yield ◽  
Chemical Fractionation ◽  
Core Proteins ◽  
Β Amyloid ◽  
Neuritic Sprouting

ABSTRACT:Purification of amyloid plaque core proteins (APCP) from Alzheimer's disease brains to complete homogeneity and in high yield permitted its chemical fractionation and characterization of its components. APCP is mainly made of β-amyloid (βA) and an assortment of glycoproteins (accounting for 20%) rich in carbohydrates compatible with N-and O-linked saccharides. When added to tissue culture of sympathetic and sensory neurons APCP and βA inhibited neuritic sprouting, a reversible phenomenon at low doses. Higher concentrations of both substances kill the neurons in culture. APCP is significantly more toxic than βA, suggesting the minor components may play an important role in increasing the toxicity of βA. If the observed toxic effects of APCP in situ are occurring in vivo during the course of AD, then the accumulation of these extracellular proteins could be largely responsible for some of the neuronal death observed in this neuropathology.

scholarly journals α-1-Antichymotrypsin Promotes β-Sheet Amyloid Plaque Deposition in a Transgenic Mouse Model of Alzheimer's Disease

2001 ◽  
Vol 21 (5) ◽  
pp. 1444-1451 ◽  
Author(s):  
Lars N. G. Nilsson ◽  
Kelly R. Bales ◽  
Giovanni DiCarlo ◽  
Marcia N. Gordon ◽  
Dave Morgan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Amyloid Plaque ◽  
Transgenic Mouse Model ◽  
Plaque Deposition ◽  
Model Of Alzheimer’S Disease ◽  
Β Sheet
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