Jürgen Götz on Gene expression profiling in the adult Down syndrome brain.

COMMENT An interesting transcriptomics study identifying differentially expressed genes and differentially regulated gene categories in Down Syndrome. Interestingly, although APP mRNA was not changed, some genes involved in APP processing (such as BACE2 and S100B

Jürgen Götz on One at a time, live tracking of NGF axonal transport using quantum dots.

COMMENT Nice study both from a technical point and as far as the scientific implications are concerned. 0 j.goetz

Jürgen Götz on Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans.

COMMENT This is an important and well-done study in human brain tissue providing support for the findings by Larry Goldstein's lab (Kamal et al., 2000; Stokin et al., 2005) that the axon is a site of Aβ production. The data are furthermore consistent with pr

Jürgen Götz on Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders.

COMMENT Excellent review discussing a whole range of abnormalities in dysfunctional mitochondria. I particularly liked the aspect on fission and fusion of mitochondria and how this is linked to apoptosis. 0 j.goetz

Jürgen Götz on Increased autophagic degradation of mitochondria in Alzheimer disease.

COMMENT These findings match with our findings of a mitochondrial dysfunction in AD, based on proteomic and functional studies (David et al., 2005). 0 j.goetz Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice.

Jürgen Götz on Soluble oligomers from a non-disease related protein mimic Abeta-induced tau hyperphosphorylation and neurodegeneration.

COMMENT I share this view. A tau pathology is seen in a range of disorders with protein aggregates rich in beta-sheet structures. A subset of patients with British dementia develop neurofibrillary tangles (NFTs) and even in prion disorders, NFT formation has been

Jürgen Götz on Single molecule profiling of tau gene expression in Alzheimer's disease.

COMMENT Holy polony....This is an ingenious approach. Also, the way the data are presented and the figures are made is a real pleasure to read. 0 j.goetz

Jürgen Götz on Somatodendritic microRNAs identified by laser capture and multiplex RT-PCR.

COMMENT Fascinating data on miRNA gradient in neurons. miRNA regulation is emerging as a new field in neurodegeneration. 0 j.goetz

Jürgen Götz on The genetics of frontotemporal lobar degeneration.

COMMENT An excellent update of the recent findings on TDP-43 and progranulin in FTD. 0 j.goetz

Jürgen Götz on Tauopathy models and human neuropathology: similarities and differences.

COMMENT A nice and comprehensive review of tauopathy models, covering species other than mice (such as C. elegans and Drosophila). 0 j.goetz

Jürgen Götz on Annonacin, a natural mitochondrial complex I inhibitor, causes tau pathology in cultured neurons.

COMMENT The study by Escobar-Khondiker and colleagues again illustrates the role mitochondrial dysfunction has in disease. The authors show that annonacin, a food toxin and complex I inhibitor that has caused an endemic to Guadeloupe, causes, in striatal cultures

Jürgen Götz on Mechanisms of mitochondrial dysfunction and energy deficiency in Alzheimer's disease.

COMMENT A very interesting review on mitochondrial dysfunction and energy hypometabolism in AD, highlighting the interaction of cellular heme and Aβ. From our own proteomics and functional studies we have evidence for a mitochondrial dysfunction in tauopathies (D

Jürgen Götz on AGEing Neurons Waste Away in Fly Model of Neurodegeneration

COMMENT Enzymes involved in glucose metabolism emerge as key players in the pathogenesis of a range of neurodegenerative disorders. Gnerer and coworkers identify a role for triosephosphate isomerase in age-related neurodegeneration in Drosophila, possibly due to

Jürgen Götz on Mutant Tau Sharpens Wits of Young Mice

COMMENT This study of a beneficial effect of tau as shown by improved long-term potentiation, in the absence of tau hyperphosphorylation, demonstrates that tau mutations, such as P301L, are not per se causing cognitive decline. As this research group has in the p

Jürgen Götz on Is Motor Neuron Axonopathy behind Movement Problems in Alzheimer Disease?

COMMENT The paper by Wirths and coworkers underscores the importance of axonopathy In Alzheimer disease. Their data obtained in APP/PS1 transgenic mice nicely extend previous findings in related animal models. Specifically, the authors refer to the findings of ax