11175 RESULTS
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
COMMENT The recent epidemiological study by Rea and colleagues adds yet more complexity (and confusion) to the issue of statin use and AD risk. It’s difficult to draw any firm conclusions from the study, since the reported outcomes vary so distinctly as a functio
COMMENT Given the termination of ADAPT, it may be many years before we know whether nonsteroidal drugs can truly inhibit or delay the onset of AD. Still, the strong observational evidence in favor of this idea warrants further investigation. Here is a paper showi
COMMENT The findings reported by Dr. Love, while having some overlap with the tissue transplant studies, show significant differences, particularly with regard to neuronal resprouting and also to the involvement of the substantia nigra. It seems likely that GDNF
COMMENT SantaCruz and colleagues manipulated transgenic tau levels using the tet-off system. Their results indicate that NFT accumulation is not sufficient to cause neuronal death and cognitive decline. This result was a bit of a surprise, because NFT formation i
COMMENT In this study, SantaCruz and colleagues have created an inducible mutant tau transgenic model, and observed the neuropathological consequences of strategically turning on and off tau expression for set periods. Profound forebrain neurodegeneration and mem
COMMENT FAD mutations inhibit cleavage at the ε site of many PS/γ-secretase substrates. Inhibition at the ε site is predicted to increase cleavage at the γ site, thus increasing Aβ production. This paper offers experimental evidence for this concept. 0 nikos.roba
COMMENT Bae et al. present compelling evidence for a crucial role of p53, a protein well-known for its role in programmed cell death, in the cellular dysfunction and associated motor abnormalities in Huntington disease (HD) (1). They establish an association betw
COMMENT The cholesterol and statin story in AD has been a never-ending battle since its inception in the late 1980s, and the current paper sends a mixed message. It seems that if the authors exclude the final year of medications from consideration, there is no re
