All Comments by Gunnar Gouras
- The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.
- Barreling Down Amyloid Plaque Distribution
- Amyloid precursor protein (APP) traffics from the cell surface via endosomes for amyloid β (Aβ) production in the trans-Golgi network.
- Epilepsy Drug Calms the Hippocampus, Aids Memory
- Modification of γ-secretase by nitrosative stress links neuronal ageing to sporadic Alzheimer's disease.
- FBL2 regulates amyloid precursor protein (APP) metabolism by promoting ubiquitination-dependent APP degradation and inhibition of APP endocytosis.
- Intracellular Aβ Causes Neurodegeneration in Mice
- Induced Neurons From AD Patients Hint at Disease Mechanisms
- Testing the right target and right drug at the right stage.
- Dynamic analysis of amyloid β-protein in behaving mice reveals opposing changes in ISF versus parenchymal Aβ during age-related plaque formation.
- Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegeneration.
- Do Overactive Brain Networks Broadcast Alzheimer’s Pathology?
- Effects of synaptic modulation on beta-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic mice.
- Deleterious effects of amyloid beta oligomers acting as an extracellular scaffold for mGluR5.
- Analysis of microdissected human neurons by a sensitive ELISA reveals a correlation between elevated intracellular concentrations of Abeta42 and Alzheimer's disease neuropathology.