Edward Koo on APP knockout attenuates microglial activation and enhances neuron survival in substantia nigra compacta after axotomy.

COMMENT What really is APP doing in vivo? One would have predicted the opposite outcome. 0 edkoo

Edward Koo on The SAMP8 mouse: a model of Alzheimer disease?

COMMENT Quite interesting if this is true. 0 edkoo

Edward Koo on Levels of nonphosphorylated and phosphorylated tau in cerebrospinal fluid of Alzheimer's disease patients : an ultrasensitive bienzyme-substrate-recycle enzyme-linked immunosorbent assay.

COMMENT A better modification of tau assay in CSF for AD diagnosis? 0 edkoo

Edward Koo on A case-control analysis of nonsteroidal anti-inflammatory drugs and Alzheimer's disease: are they protective?

COMMENT I wonder if this study can be reinterpreted to say that recent NSAID exposure is no use in AD prevention. If the data from others that AD starts years to decades earlier is true, then NSAID likely will have to be given far earlier than the 3 years period

Edward Koo on Mapping the evolution of regional atrophy in Alzheimer's disease: unbiased analysis of fluid-registered serial MRI.

COMMENT Further evidence that imaging can be a surrogate marker of ad progression. But can this be a rapid and reliable instrument in other hands? 0 edkoo

Edward Koo on Mutant ubiquitin found in neurodegenerative disorders is a ubiquitin fusion degradation substrate that blocks proteasomal degradation.

COMMENT More evidence that the +1 mutations causes cell dysfunction. 0 edkoo

John Hardy on Identification of a novel family of presenilin homologues.

COMMENT While the homology between these proteins and PS1 and PS2 is not great, their importance is that their occurrence suggests there may be many other regulated membrance cleavage pathways and detailed comparisons may also give mechanistic insights into the c

Edward Koo on Postischemic hyperthermia induces Alzheimer-like pathology in the rat brain.

COMMENT Based on previous studies on brain trauma, these results are not surprising. What is surprising is that if a human specific abeta antibody is used, then it should not pick up rodent abeta as these are not transgenic animals. 0 edkoo

Edward Koo on Alpha-synuclein-immunoreactive deposits in human and animal prion diseases.

COMMENT Curious why synuclein seems to be associated with some (non-lewy body) neurodegenerative disorders but not others. I would be interested to see if the same is seen in the british and danish bri-associated dementias. 0 edkoo

Edward Koo on Peeling plaque. Researchers remain optimistic about a vaccine against Alzheimer's.

COMMENT Interesting commentary. 0 edkoo

Edward Koo on FAD mutant PS-1 gene-targeted mice: increased A beta 42 and A beta deposition without APP overproduction.

COMMENT Lovely study to show that under the right circumstances, overexpression of neither ps1 mutation nor app is required to generate amyloid deposition in brains of transgenic mice. The usual massive overexpression of app required to induce amyloid deposition

Benjamin Wolozin on Aggregation of alpha-synuclein induced by the Cu,Zn-superoxide dismutase and hydrogen peroxide system.

COMMENT There appears to be a strong connection between metals and synuclein aggregation. Kang's group previously showed that copper and iron potently stimulates synuclein aggregation in vitro, and papers from my group have shown that iron stimulates synucle

Benjamin Wolozin on Poly-L-lysine dissolves fibrillar aggregation of the Alzheimer beta-amyloid peptide in vitro.

COMMENT Advisor Comment: Developing compounds to inhibit Aβ aggregation, or to resolubilize aggregated Aβ

Benjamin Wolozin on Brain to plasma amyloid-beta efflux: a measure of brain amyloid burden in a mouse model of Alzheimer's disease.

COMMENT It has previously been postulated that there is efflux of Aβ from the CNS to the periphery. This paper elegantly shows that this is the case, and in the process suggests a possible plasma test for assessing the CNS amyloid burden in Alzheimer patients. 0

Benjamin Wolozin on Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.

COMMENT Previous work by the labs of Klein and Krafft showed that synthetic Aβ aggregates, termed ADDLs, are highly toxic and inhibit hippocampal function. This work now elegantly shows that Aβ oligomers generated in cells are also toxic. One puzzling aspect of t