It's almost time for the 2017 Society for Neuroscience meeting. To get your neurons excited for the meeting, here's a journal club discussing a recent paper with interesting findings for Alzheimer's disease.
The pathological hallmark of Alzheimer’s disease (AD) is the accumulation of amyloid β (Aβ) plaques and neurofibrillary tangles. Despite decades of research, the direct (and indirect) contribution of these lesions in disease progression is poorly understood. Do these lesions directly cause neuronal dysfunction and neurodegeneration? If so, why do some patients accumulate these lesions, but exhibit normal neurological behavioral before death? Do AD patients have secondary defects in cellular and/or molecular processes that normally function to protect patients from accumulation of these nefarious lesions? If so, what are these cell types and what…
Take a breath.