Excess betaCTF, not Abeta: the culprit in Alzheimer-related endocytic dysfunction
- PMID: 20133888
- PMCID: PMC2824414
- DOI: 10.1073/pnas.0913922107
Excess betaCTF, not Abeta: the culprit in Alzheimer-related endocytic dysfunction
Conflict of interest statement
The author declares no conflict of interest.
Comment on
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Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition.Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1630-5. doi: 10.1073/pnas.0908953107. Epub 2009 Dec 28. Proc Natl Acad Sci U S A. 2010. PMID: 20080541 Free PMC article.
References
-
- Tanzi RE, et al. Protease inhibitor domain encoded by an amyloid protein precursor mRNA associated with Alzheimer’s disease. Nature. 1988;331:528–530. - PubMed
-
- Mrak RE, Griffin WS. Glia and their cytokines in progression of neurodegeneration. Neurobiol Aging. 2005;26:349–354. - PubMed
-
- Barger SW, Harmon AD. Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E. Nature. 1997;388:878–881. - PubMed
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