For generations of neuroscientists, using immunohistochemistry to study the brain in its anatomical context typically meant imaging a tiny slice at a time. Using the traditional method of taking micron thick sections, fixing, staining, imaging, and, finally, stitching all the slices together, is a super laborious task, especially for large tissues. But what if you could "look" into an intact mouse brain and identify specific cells and eliminate all of the slicing and stitching?
You might be surprised to learn that diabetes, a metabolic disease, may be linked to the neurodegenerative condition Alzheimer’s disease (AD). Diabetes is driven by altered insulin signaling from either insufficient insulin production (Type 1) or altered insulin receptor (IR) signaling (Type 2). In a seemingly unrelated disease, the human e4 allele of APOE is the strongest genetic risk factor for AD.
In Nov 2017, over 30,000 neuroscientists gathered in Washington D.C. to talk all things brain at the Society for Neuroscience (SfN) meeting. I’ve attended SfN for what is now on the order of decades. Having reluctantly accepted veteran status for the annual meeting, I thought this year’s SfN was an opportunity to consider where neuroscience has been, where it is, and where it’s going.
The research objectives at SfN — to understand how molecules, cells, and circuits drive complex behavior — are broad and overwhelming. Even today, I choke up recalling that inevitable question I’d get from my graduate school advisor after a meeting — what did you learn? Such a question is challenging for any meeting, and a strong perspective, particularly for SfN, is necessary to even consider it.
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.