11633 RESULTS
COMMENT These papers, dealing with an effect of Aβ on postsynaptic mechanisms, when considered in combination with the recent paper from the Ferreira lab which shows an effect of Aβ on presynaptic mechanisms, show that there is more than one target through which
COMMENT This interesting hypothesis may well explain the apparent discord between human observational and trial results with hormone therapy. There may be other biological explanations, but any of these are more interesting and potentially valuable than to write
COMMENT I found this paper fascinating and very intriguing, but could not determine whether the effects attributed to lowered tau levels (from the otherwise very high levels) are instead due to a neuroprotective effect of the drug used to control tau expression.
COMMENT Kang and colleagues described a new role of presenilins on the highly conserved ERK signaling cascade. Specifically, these authors demonstrate that loss of presenilins alters the expression, degradation, and function of the tyrosine kinase receptor PDGF,
COMMENT Kang and co-workers examined the effect of PS1 and PS2 deficiency on PI3/Akt and ERK pathways, highlighting the importance of upstream cell-surface receptors in PS1- and PS2-mediated Akt and ERK signaling. The authors demonstrate that the loss of PS1 and
COMMENT The elegant series of experiments by Yang et al. provide compelling evidence that increased serum retinol binding protein 4 is an important contributor to the pathogenesis of insulin resistance that is associated with a variety of genetic and environmenta
COMMENT This report from Akbar and Kim adds to their earlier work in this area by providing compelling evidence for an impact of DHA on enhancing the rate of PI3K>Akt signaling in neurons and brain by increasing phosphatidylserine (PS) and translocation-depend
COMMENT Neurofibrillary Tangles: Villain or Merely Vilified? What’s Next? TADDLs/TAuDDLs! For most investigators in the field of Alzheimer disease (AD), pathology has become equated with pathogenesis. As such, the two leading theories concerning the disease revol
COMMENT These two papers from the Greengard and Gouras labs identify specific pre- and postsynaptic defects in cultured neurons induced by exposure to the β-amyloid peptide (Aβ). It is well-established that synaptic loss likely occurs early in the Alzheimer patho
COMMENT This looks like progress. DONCROWNPOINT 0
COMMENT About 40 years ago, Joseph Altman and his colleagues used the 3H-thymidine autoradiographic method to birthdate cells in the brains of adult rats and cats, and reported evidence for neurogenesis in the olfactory bulb, hippocampus, and neocortex (1-5). The
COMMENT I would be interested in how the community thinks this study ties in with the prescription of memantine (an NMDA-receptor antagonist) for moderate to severe Alzheimer disease. If NMDA receptor deficits contribute significantly to Alzheimer disease, would
COMMENT The authors test the association between cognitive impairment (CI) with and without subcortical vascular abnormalities (SF) and insulin resistance (IR) in a cross-sectional population-based study. Geroldi et al. subdivided their CI patients between a larg
COMMENT These papers provide intriguing evidence for a link among β-amyloid, excitatory synaptic transmission, and altered membrane trafficking. It has been known for some time that early stages of Alzheimer disease (AD) are associated with learning impairments a
COMMENT These are very interesting studies. There has been growing evidence that some of the primary targets of AD and APP are synapses. These studies support this view. Furthermore, there has been recent interest in the relation between APP processing and synapt
