11617 RESULTS
COMMENT In our paper last year (Desai et al., 2002), we did not see any association of this intronic polymorphism with late-onset AD in our case-control cohort. One of the obvious differences between our study and this one is that our American White sample size w
COMMENT The quantitative analyses of volumes of different brain structures in an APP mutant mouse line by Redwine et al. provide valuable new information concerning the possible relationships between altered APP processing, amyloid deposition, and cellular damage
COMMENT The analyses of mice with adipose cell-specific knockout of the insulin receptor (FIRKO mice) by Bluher et al. provide at least three major advances in our understanding the mechanisms whereby insulin signaling and energy metabolism regulate life span. Fi
COMMENT Having been a neurologist in a former life, I have always wondered about how much aging plays a role in the neurodegenerative disorders. For some time it seemed that the debate (for it was a debate with little real information) fell into two categories. O
COMMENT Papassotiropoulos et al. have described the association of an intronic polymorphism in the CYP46 gene with AD. They found this polymorphism to influence Aβ load, however, the authors failed to show an effect on cholesterol or 24S-hydroxycholesterol CSF le
COMMENT The increased production of Aβ in Alzheimer’s disease is acknowledged to be a key pathogenic event. It is becoming apparent that Aβ itself is neurotoxic, without necessarily involving the amyloid in plaques (Small et al., 2001). For this reason, identifyi
COMMENT Phospho-state-specific antibodies have played a major role in molecular neuropathology for many years. Some of these antibodies have been monoclonals, generated by immunizing with tissue extracts and then screening for certain histochemical properties (e.
COMMENT This article presents a novel regulatory mechanism for APP processing. Li et al. observe that increased expression of SUMO-3 increases production of Aβ and reduces production of APPsα. SUMO (small ubiquitin-like modifier) proteins are small peptides that
COMMENT The findings by Li et al. on the regulation of APP processing by sumoylation indeed bring a new perspective to the field of AD research. Although the authors documented a lack of direct sumoylation of APP and BACE, they have demonstrated a clear increase
COMMENT We appreciate the comment by Jose Luchsinger and Richard Mayeux. We did not include the results of
COMMENT This is a beautiful study aimed at unraveling the connection between ApoE, a prominent risk factor for AD, and intracellular signaling and tau phosphorylation. Immunohistochemistry would have been very useful in the interpretation. Perhaps the authors are
COMMENT This is a fascinating study that uses an in vivo model to explore the role of cell cycle regulators in neurodegeneration. I was unable to download the full paper, and so I'm curious to find out why MPM2 immunoreactivity was not observed. Might it be
COMMENT Neuronal dystrophy and Aβ deposition are major pathological features of AD. Previous work has established the association of neuronal dystrophy with synaptic loss in the Alzheimer's brain (Terry et al., 1991), and cultured neurons (Grace et al., 2002
COMMENT This paper is indeed a very interesting publication that once more demonstrates the power of mass spectrometry in biochemical study when combined with other molecular approaches. This paper reported a new method to study tyrosine phosphorylation profiles
COMMENT This convincing report provides integrated DNA, RNA, and protein data that is used for disease gene discovery in a rare form of a mitochondrial disorder named Leigh syndrome, an autosomal recessive cytochrome c deficiency. Specifically, the authors combin
