41 RESULTS
COMMENT Once again, I feel compelled to point out that TFEB has been connected to APOE genotype in AD. Essentially, compelling evidence indicates that ApoE4 binds (evidently, with higher affinity than ApoE3) to the "CLEAR" enhancers that comprise the ...
COMMENT This is quite intriguing. I wonder if the association might have anything to do with APOE genotype? I'm rather surprised that the study did not include analysis of that variable. ApoE isoforms have been shown to impact personality traits when ...
COMMENT In their article, Konttinen et al. write: "[E]xact mechanisms underlying human APOE4-induced inflammatory phenotype in AD microglia remain incompletely defined." Their study and several other recent publications suggest a strong possibility of a ...
COMMENT Regarding ApoE and autophagy, it appears the mechanism is a surprising one. A few years ago, Dale Bredesen and colleagues strengthened the evidence for ApoE being found intracellularly, in the nucleus and bound to DNA, in fact. As it turns out, the DNA ...
COMMENT This is a tour de force, integrating many sophisticated forms of analysis. In the context of many other indices of neuroinflammation and microglial malactivation, the evidence that these cells participate in AD progression is difficult to refute. ...
COMMENT The link between APOE genotype and autophagy has recently received mechanistic reinforcement. We have demonstrated avid, specific binding of ApoE to DNA elements known as "CLEAR" sites, the cis elements bound by transcription factor EB (TFEB), a ...
COMMENT Interesting and perhaps related: It has been known for some time that extracellular UPS components are present and functional (Sixt et al, 2008), including in cerebrospinal fluid (Mueller et al., 2012). This may reflect favorably on Model 2 proposed by ...
COMMENT This study by Woodruff et al. has provided intriguing new ideas about the roles of enzymes that have previously garnered interest almost exclusively due to their effects on APP. BACE1 and γ-secretase are well-known to have effects on other substrates, and ...
COMMENT There was a really small difference in the exercise levels reported to confer risk. And I take issue with the claim by the paper's authors, and the reporting in this Alzforum article, that patients and controls differed in the number of times per ...
COMMENT Joachim Herz and his lab have accomplished a milestone in research on the biology of reelin, a protein that has complex biochemistry and genetic contributions to brain development, as well as synaptic plasticity in the adult. Because it is so critical for ...
COMMENT This is a fascinating body of work. It should be noted that it is corroborated also by Sala-Llonch et al., 2015. That study had the additional strengths of being longitudinal and including initially asymptomatic carriers of nine different PSEN1 mutations ...
COMMENT Excitatory amino acids (EAA) have a long and complex history in AD research. Considerable evidence exists for EAA dysregulation in AD pathogenesis, including depletion of the so-called “glycine B ” component of the NMDA receptor (Procter et al., 1989). ...
COMMENT It seems the following papers would be relevant to the C9ORF72 data: Bieniek et al., 2013; King et al., 2013. bargerstevenw 0 Tau pathology in frontotemporal lobar degeneration with C9ORF72 hexanucleotide repeat expansion. Mixed tau, TDP-43 and p62 ...
COMMENT This confirms a hypothesis that I invoked to explain the results of a study in which I was involved, that examined the role of D-serine in ALS. D-Ser is a co-agonist at the NMDA-R "glycine" site, and is likely to be the most important agonist in ...
COMMENT This is a fascinating report that seems to help clarify the roles of inflammation-related immune agents in AD. There has been some confusion and controversy arising from the findings that innate immune reactions appear to contribute to the development of ...
