11178 RESULTS
COMMENT This is the first paper to show (11)C-PiB binding in PET in hereditary cerebral amyloid angiopathy and APP locus duplication. The paper reports increased uptake of (11)C-PiB in the striatum and the posterior cingulate in two cases with APP duplication, wh
COMMENT In agreement with Dr. Vassar’s comments, the two inhibitors used in Dr. Hook’s study, CA074-Me and
COMMENT In a separate discussion, Dr. Vassar cites McConlogue et al. (2008), which shows that knocking out BACE1 in mice expressing human APP containing the wild-type β-secretase site (PDAPP) significantly reduces Aβ and amyloid plaques in support of his conclusi
COMMENT The experiments described by Head et al. may not elucidate the role played by senile plaques in AD dementia, but they do bolster the idea that amyloid disruption therapy is likely to be most efficacious when administered early in the course of the disease
COMMENT Therapeutic vaccination trials in Tg animals and humans have revealed that senile plaques, a cardinal pathologic feature of AD, are dynamic structures subject to dissolution by Aβ immunotherapy. Although Aβ deposits are a logical AD therapeutic focus, it
COMMENT This is a fascinating paper from the group of Mathias Jucker and Michael Calhoun studying in vivo interaction of amyloid plaques and their most intriguing and prominent cellular component—the microglia. Employing two-photon imaging of GFP-labeled microgli
COMMENT This is an excellent review for those interested in the role of obesity, insulin resistance, and diabetes in AD. This is an important research area as the population ages and obesity and diabetes are on the rise. The explanation of terms such as glucose i
COMMENT The paper by Bolmont and colleagues (2008) represents an elegant set of experiments designed to track microglia in a doubly-transgenic mouse model of AD. The authors crossed an Iba1-GFP transgenic (thereby labeling microglia green) with a co-injected APP/
COMMENT This paper illustrates nicely how complex and dynamic the interactions between microglia and β amyloid are, and how relevant these interactions are to the pathogenesis of Alzheimer disease, at least in mouse models. The paper supports a role for microglia
COMMENT I appreciate Dr. Vassar’s comment posted in response to my comment based on our new article, which
COMMENT These studies elegantly demonstrate that transplanted fetal grafts can survive and thrive in human brains for prolonged periods, clearly moving the field in new, exciting directions. However, the view that the presence of α-synuclein in these grafted neur
COMMENT I think the impression created by the Li and Kordower papers that there is “PD pathology in the transplants ” is unfortunate. The papers give the impression of an “either/or” proposition of "pathology" in the transplant cases, but neither paper
COMMENT In an elegant series of studies, one mechanism through which Aβ oligomers may cause synaptic dysfunction may be disruption in phophatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) metabolism. The authors show that oligomeric Aβ destabilizes and reduces Ptd
COMMENT Capacity for consent is a thorny ethical issue in dementia research. This paper is a useful step toward establishing standardized criteria for evaluating capacity in patients involved in clinical trials. 0 lwalker
COMMENT I'd like to discuss the similarities between data generated in APP/Tg mice vaccinated with an AD vaccine, AN1792 trials, and results reported here in canines by Head and coauthors. Experimental dogs immunized 25 times with a high dose (500 mg/injecti
