48 RESULTS
COMMENT Together with their previous study (1), this paper from the Steinman group leaves little doubt that Aβ peptides (both 40 and 42) exert beneficial effects in the EAE mouse model of MS; they do so by reducing neuroinflammation and attenuating paralysis. The
COMMENT Treating a disease at early stages certainly increases the chances of a successful outcome. However, based on the following reasons, I think there are drawbacks associated with the approach (testing the anti-amyloid therapies in asymptomatic individuals),
COMMENT The finding that ApoE4 carriers display Aβ-independent pathomechanisms is not really surprising. To give a few examples of Aβ-independent effects of ApoE4, the literature shows that ApoE4 carriers also have poor outcome following traumatic brain injury, a
COMMENT 2, and comments by Daniel Davis on the paper. Therefore, practically speaking, we need a therapeutic
COMMENT Michael Heneka’s comment above). As Neumann and Daly pointed out in their NEJM commentary, amyloid plaques
COMMENT This study from the Checler group provides compelling evidence that 3xTg mice accumulate the C99 fragment of APP and not Aβ at a young age (three to six months). It is likely that these results may not bring an end to the ongoing debate regarding the pres
COMMENT This study by Bali et al. provides compelling evidence that downregulation of the late-onset AD (LOAD) risk genes in cell cultures does not alter Aβ generation in a pathologically meaningful way, and suggests that increased Aβ42 levels or Aβ42/40 ratio ma
COMMENT This study provides elegant genetic evidence that reducing the BACE processing of APP protects against late-onset AD. The finding complements the long-standing observations that increased BACE processing (APPswe mutation or elevated BACE levels [1]) enhan
COMMENT Coming hard on the heels of the work by Brunden and colleagues (Zhang et al., 2012), this study further strengthens the validity of microtubules as a therapeutic target for the treatment of AD. Although most of the preclinical data are obtained by studyin
COMMENT warrants comment. This is a new antibody and is relatively unknown to the AD field. Having an IgG4
COMMENT The conclusion that elevated CSF p-tau levels with reduced Aβ levels (Aβ+/p-tau+) are better correlated with clinical decline in baseline CDR = 0 (cognitively normal) individuals will help the pharmaceutical industry/clinical researchers better stratify s
COMMENT These conclusions are based on a four-month treatment, whereas most trials go on for 18 months, and some even for 36 months. Knowing the complexity of AD pathogenesis, would a four-month treatment be considered sufficiently long to test the efficacy of an
COMMENT Sperling et al. have put forward a now familiar argument (also proposed by others; 1-4) that amyloid-based therapies of the past decade have failed not because they were targeted at the wrong pathophysiological mechanism, but rather because the interventi
COMMENT Alzforum should be commended for highlighting the ACCORD MIND study. At first glance, the findings from this study (an aggressive treatment to control diabetes did not improve cognition and in fact may be detrimental) seem to lack direct relevance to AD,
COMMENT In my view, the importance of this study lies in the finding that APP-induced neurodegeneration is cell autonomous. This study makes clever use of cell-specific promoters to show that only the APP-overexpressing cells undergo apoptosis while the neighbori
