80 RESULTS
COMMENT I have known Dr. Peter Davies for more than 30 years. I first met him in 1986 at a Bunbury Symposium on the Molecular Neuropathology of Aging that he organized at Cold Spring Harbor Laboratories. Peter made significant and lasting contributions to the neu
COMMENT This study is a significant contribution. It represents the culmination of research started in 1993, when Dr. Pappolla started a collaboration with me and Dr. Sambamurti in my laboratory. I trust that with this determined pursuit, the study will lead to a
COMMENT This is a very important paper from Dr. Pappolla and associates. It demonstrates for the first time that the lymphatic system may play a substantive role in the clearance of Aβ peptides from the brain. Impaired clearance of amyloid may play a major role i
COMMENT This is a very interesting work, showing for the first time that increasing neuronal cAMP prevents caspase activation, tau cleavage, and neuronal cell death. The data in the paper support the suggestion that increasing proteasome activity in a sustainable
COMMENT The commentary by Sperling and colleagues is thought provoking and a welcome addition to a longstanding and important scientific debate. Regardless of the disappointing results of the clinical trials of anti-amyloid drugs, however, there are strong ration
COMMENT The current debate catalyzed by the important paper of Winton et al. highlights a serious concern facing the AD field, namely, the relevance of transgenic animal models to the neurodegeneration of AD, the real cause of dementia. Most transgenic models cur
COMMENT I find this paper interesting, as it reports evidence that Aβ oligomers may cause dementia by ultimately inhibiting functions of NMDA receptor, a factor that functions in memory. Importantly, the described work predicts that additional Alzheimer’s disease
COMMENT This study is interesting in that it shows that patients with familial hypercholesterolemia have high incidence of mild cognitive impairment (MCI). The report suggests that exposure to elevated cholesterol during middle age or earlier or dysfunction of li
COMMENT The paper by Inoue et al. adds important new evidence to the synaptic function of EphA4, a receptor involved in the development and function of the CNS. In addition, it verifies reports that PS1 is localized at synaptic contacts (Georgakopoulos et al., 19
COMMENT This paper shows the generation of a novel model of cerebral (non-Aβ) amyloid deposition. The authors generated transgenic mice expressing a mutant form of the BRI gene, found in patients affected by familial Danish dementia (FDD). FDD is a rare inherited
COMMENT In the last years, several laboratories have shown experimentally that presenilin FAD mutations cause a loss of function in both γ-secretase-dependent (Chen et al., 2002; Marambaud et al., 2003; Georgakopoulos et al., 2006) and γ-secretase-independent (Ka
COMMENT The paper by Doglio et al. has important implications for both the biological functions of the presenilin (PS) complex and the mechanisms by which PS FAD mutations promote neurodegeneration and other structural abnormalities in AD. The paper verifies prev
COMMENT This is a very interesting paper. It indicates that loss of PS1 function may lead to plaque pathology and amyloid depositions. The authors conclude that it is the loss of the γ-secretase function of PS1 and the reduction of Aβ1-40 that lead to increased p
COMMENT Many Mechanisms to Gain Aβ and Its Uncertain Role in AD Peter’s comments are very well taken.
COMMENT The concept of this study could be important, as it may offer an explanation for tau overphosphorylation in AD. On the other hand, it is not clear how this theory explains the independent distribution of the amyloid plaques and neurofibrillary tangles (NF
