Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

1996 ◽  
Vol 2 (8) ◽  
pp. 864-870 ◽  
Author(s):  
D. Scheuner ◽  
C. Eckman ◽  
M. Jensen ◽  
X. Song ◽  
M. Citron ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Presenilin 1 ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Β Protein ◽  
Familial Alzheimer's Disease

The genetic defect in familial Alzheimer's disease is not tightly linked to the amyloid β-protein gene

Nature ◽  
1987 ◽  
Vol 329 (6135) ◽  
pp. 156-157 ◽  
Author(s):  
Rudolph E. Tanzi ◽  
Peter H. St George-Hyslop ◽  
Jonathan L. Haines ◽  
Ronald J. Polinsky ◽  
Linda Nee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Gene ◽  
Genetic Defect ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Β Protein ◽  
Familial Alzheimer's Disease

scholarly journals Effects of Familial Alzheimer’s Disease Mutations on the Folding Nucleation of the Amyloid β-Protein

2008 ◽  
Vol 381 (1) ◽  
pp. 221-228 ◽  
Author(s):  
Mary Griffin Krone ◽  
Andrij Baumketner ◽  
Summer L. Bernstein ◽  
Thomas Wyttenbach ◽  
Noel D. Lazo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Disease Mutations ◽  
Β Protein ◽  
Familial Alzheimer's Disease

scholarly journals Aluminum and Tau in Neurofibrillary Tangles in Familial Alzheimer’s Disease

2021 ◽  
pp. 1-12
Author(s):  
Matthew John Mold ◽  
Adam O’Farrell ◽  
Benjamin Morris ◽  
Christopher Exley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Phosphorylated Tau ◽  
Familial Alzheimer’S Disease ◽  
Therapeutic Benefits ◽  
Familial Alzheimer's Disease

Background: Familial Alzheimer’s disease (fAD) is driven by genetic predispositions affecting the expression and metabolism of the amyloid-β protein precursor. Aluminum is a non-essential yet biologically-reactive metal implicated in the etiology of AD. Recent research has identified aluminum intricately and unequivocally associated with amyloid-β in senile plaques and, more tentatively, co-deposited with neuropil-like threads in the brains of a Colombian cohort of donors with fAD. Objective: Herein, we have assessed the co-localization of aluminum to immunolabelled phosphorylated tau to probe the potential preferential binding of aluminum to senile plaques or neurofibrillary tangles in the same Colombian kindred. Methods: Herein, we have performed phosphorylated tau-specific immunolabelling followed by aluminum-specific fluorescence microscopy of the identical brain tissue sections via a sequential labelling method. Results: Aluminum was co-localized with immunoreactive phosphorylated tau in the brains of donors with fAD. While aluminum was predominantly co-located to neurofibrillary tangles in the temporal cortex, aluminum was more frequently co-deposited with cortical senile plaques. Conclusion: These data suggest that the co-deposition of aluminum with amyloid-β precedes that with neurofibrillary tangles. Extracellularly deposited amyloid-β may also be more immediately available to bind aluminum versus intracellular aggregates of tau. Therapeutic approaches to reduce tau have demonstrated the amelioration of its synergistic interactions with amyloid-β, ultimately reducing tau pathology and reducing neuronal loss. These data support the intricate associations of aluminum in the neuropathology of fAD, of which its subsequent reduction may further therapeutic benefits observed in ongoing clinical trials in vivo.

scholarly journals Familial Alzheimer’s Disease Mutations Differentially Alter Amyloid β-Protein Oligomerization

2012 ◽  
Vol 3 (11) ◽  
pp. 909-918 ◽  
Author(s):  
Megan Murray Gessel ◽  
Summer Bernstein ◽  
Martin Kemper ◽  
David B. Teplow ◽  
Michael T. Bowers
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Protein Oligomerization ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Disease Mutations ◽  
Β Protein ◽  
Familial Alzheimer's Disease
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