In mice, the presence of mutant human tau disrupts synaptic signaling and slows down neuronal firing.
The Journal of Neuroscience retracted a paper that claimed Aβ does not accumulate inside neurons, and temporarily banished its senior authors.
Researchers at a Keystone meeting proposed that quelling inflammation outside the brain could slow the progression of Alzheimer’s and other neurodegenerative diseases.
Whether cleaning up plaques in AD or mopping up debris in the wake of a stroke, microglia get by with a little help from TREM2.
Large consortium releases epigenome profiles of 111 different tissues. They are already yielding insight into the immune system’s role in Alzheimer’s disease.
Skin side effect under investigation.
Routine cognitive screening could help doctors spot people at risk of dementia. Two new tests could make screening more accessible.
A debate has sprung up in response to a Cell essay arguing that the baby was thrown out with the bathwater when a γ-secretase inhibitor failed in Phase 3.
"Non-Motor Symptoms: Unraveling the 'Invisible' Face of Parkinson’s Disease," will be held on April 27 2015, at the New York Academy of Sciences in lower Manhattan. Abstracts must be received by Friday, March 13. For more information, and to register, please visit the conference website.
When the γ-secretase inhibitor semagacestat sank ingloriously over side effects and cognitive worsening in Phase 3 testing, small-molecule drug developers tossed the target onto the scrap heap and turned their focus and resources toward BACE. But wait—semagacestat is history, but has the field at large learned enough from the data to warrant giving up on γ-secretase, too? Prompted by Bart De Strooper, leading scientists in academia and industry are debating the question. Read De Strooper’s article, generously made available by Cell Press. Ponder the extensive commentary on Alzforum, consider the detailed reply by Eric Siemers and colleagues at Eli Lilly and Company, and join the conversation.
What distinguishes a hippocampal neuron from a substantia nigra one—or from a liver or blood cell, for that matter? It’s all in the parts of the genetic code they choose to read or ignore, determined by epigenetic markers like histone methylation. Now scientists can read the epigenome too, in a publicly available set of reference data from 111 different tissue types. The data suggest that changes to gene expression in immune cells initiate Alzheimer’s disease.
Berislav Zlokovic's recent Neuron paper set the stage for Alzforum’s latest Webinar, "Leaky Blood-Brain Barrier: A Harbinger of Alzheimer's?" Borrowing an MRI technique from oncology to measure the permeability of the BBB, Zlokovic and colleagues reported an age-related breakdown of the barrier in older adults and in people with mild cognitive impairment. Tammie Benzinger, Roderick Corriveau, and Costantino Iadecola joined Zlokovic for a panel discussion. If you missed the Webinar, you can catch it all online. The recording and slide presentation are now available.
- Gunnar Gouras on Mistakes Prompt Retraction of Controversial Paper, and Publication Ban
- Takaomi Saido on Mistakes Prompt Retraction of Controversial Paper, and Publication Ban
- Thomas Bayer and Oliver Wirths on Mistakes Prompt Retraction of Controversial Paper, and Publication Ban
- Charles Glabe on Lessons from a failed γ-secretase Alzheimer trial.
- Michael Heneka on TREM2 Lipid Sensing Sustains the Microglial Response in an Alzheimer's Disease Model.
- Rebecca Sims on Consortium Debuts Biggest Set of Human Epigenomes To Date
- Eric Siemers, Ronald DeMattos, Robert Dean and Karen Sundell on Lessons from a failed γ-secretase Alzheimer trial.