25 RESULTS
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COMMENT This is a fascinating and very significant study by Yambire et al. that, I think, has important implications for understanding the molecular mechanism by which mutations in the PRESENILIN genes, and possibly APP, contribute to early onset familial ...
COMMENT Although I am a minor co-author on this paper, I would, nevertheless, like to comment on it to point out how very significant I think it is. In 2016 I published, with others, a review on the role of the presenilin genes in early onset familial AD (Jayne ...
COMMENT This commentary is a clear and important critique of the attempt to redefine Alzheimer's disease in the "NIA-AA Research Framework." As a senior colleague stated when I showed it to him: "It is rare that anything is achieved by the ...
COMMENT This paper is particularly interesting due the effects the authors observed of inhibiting β-secretase in iPSC neurons carrying fAD mutations. The authors observe that fAD mutations in either APP or PSEN1 cause defective degradation of autophagosomes. ...
COMMENT The intense focus of the AD research community on the function of the APP gene has revealed an astonishingly complex combination of regulatory mechanisms involving transcription, mRNA stability, translation, and protein stability. Many of these mechanisms ...
COMMENT This is a detailed analysis of the role of Aβ in Alzheimer’s disease and the justification for defining Alzheimer’s disease by the presence of Aβ, with supplementary information to extend particular arguments. It traces the historical development of ...
COMMENT This paper and others recently published (see below) illustrate the critical role played by APP in the regulation of cellular iron homeostasis. APP translation is controlled by the binding to its mRNA of Iron Regulatory Protein 1 (IRP1). Using SH-SY5Y ...
COMMENT With this paper, I think Area-Gomez, Schon, and coworkers have made a real advance in our understanding of APP’s role in Alzheimer’s disease. They show that the increased apposition of the ER and mitochondria due to lack of PSEN activity (and as seen in ...
COMMENT Reading the title of this paper might mislead people to think that there is evidence that zebrafish produce a peptide similar to Aβ. However, while there are two “co-orthologues” of the APP gene in zebrafish (appa and appb), Aβ peptides cleaved from the ...
COMMENT This very significant paper refutes one of the most “beautiful” sets of data supporting the amyloid hypothesis—the correlation between Aβ40:42 ratio and the mean age at onset of AD for FAD mutations in PSEN1. Figure 5 is particularly worthy of note both ...
COMMENT Hargis and Blalock have analyzed publicly available transcriptome data from humans and rodents and from purported transgenic rodent models of Alzheimer’s disease to assess whether the transgenic rodents are, in fact, modelling the disease. They found good ...
COMMENT I was curious to see that this paper did not address the previous observations of Area-Gomez et al. (2009) that a major site of subcellular localization of PSEN2 is the mitochondria-associated membranes of the ER, at least in mouse brain. Since the ...
COMMENT It is fascinating to follow this debate between the teams of De Strooper/Chávez-Gutiérrez and Shen/Kelleher. The technical arguments presented by both teams in the discussion sections of their recent papers in Neuron are valuable information. However, ...
COMMENT This very interesting paper continues the work of the Schon laboratory investigating the role that the mitochondrial-associated membranes (MAM) of the endoplasmic reticulum may play in Alzheimer's disease. Schon and co-workers have previously shown ...
COMMENT Xia and co-authors should be commended for examining the function of familial AD (FAD) mutations in PSEN1 in a very physiologically relevant model system. Their observation of loss of γ-secretase activity for FAD mutations engineered into in mouse Psen1 ...
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