New hypothesis for amyloid ??-protein in Alzheimer's disease

1992 ◽  
Vol &NA; (853) ◽  
pp. 2
Author(s):  
&NA;
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Protein ◽  
New Hypothesis

A New Hypothesis of Pathogenesis Based on the Divorce between Mitochondria and their Host Cells: Possible Relevances for the Alzheimer's Disease

2010 ◽  
Vol 999 (999) ◽  
pp. 1-16 ◽  
Author(s):  
L.F. Agnati ◽  
D. Guidolin ◽  
F. Baluska ◽  
G. Leo ◽  
P.W. Barlow ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Host Cells ◽  
New Hypothesis

scholarly journals TMCC2 Associates with Alzheimer's Disease Pathology

2021 ◽  
Author(s):  
Paul C R Hopkins ◽  
Claire Troakes ◽  
Guy Tear
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apoe Genotype ◽  
Coiled Coil ◽  
Amyloid Protein ◽  
Neuritic Plaques ◽  
Protein Precursor ◽  
Apoe Isoforms ◽  
First Time ◽  
Differential Affinity

We previously identified Transmembrane and Coiled-Coil 2 (TMCC2) as a protein that forms complexes with both apolipoprotein E (apoE) and the amyloid protein precursor (APP) and which displayed differential affinity for apoE isoforms apoE3 and apoE4. Here we have for the first time examined TMCC2 in the human brain and found that it is affected by APOE genotype and brain region. We further observed that TMCC2 associates with the pathology of Alzheimer's disease in dense core and neuritic plaques. TMCC2 is therefore positioned to mediate impacts of apoE4 on Alzheimer's disease pathology.

scholarly journals Fleshing out the amyloid cascade hypothesis: the molecular biology of Alzheimer's disease

2000 ◽  
Vol 2 (2) ◽  
pp. 101-110 ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Biology ◽  
Basic Science ◽  
Amyloid Protein ◽  
Amyloid Cascade Hypothesis ◽  
Protein Tau ◽  
Disease Modifying Therapies ◽  
Disease Modifying ◽  
Amyloid Cascade

Alzheimer's disease (AD) is a disorder of two pathologies- plaques and tangles. The former have as a key constituent amyloid protein and the latter the microtubule-associaied protein tau. Genetics has demonstrated that changes in either protein are sufficient to cause dementia. The amyloid cascade hypothesis proposes that plaque-related changes precede tangle-related changes and positions amyloid as central to the degeneration of AD. All the evidence suggests this is correct, including evidence that presenil ins alter the processing of the amyloid precursor protein and evidence that disrupting the normal properties of tau underlies the related froniotemporal dementias. The amyloid cascade hypothesis has provided the basis for nearly a decade of intensive basic science - the skeleton of that hypothesis can now be fleshed out, and confidence is growing that this will result in useful disease-modifying therapies in the future.

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