Seizures in AD mice lead to cognitive changes via epigenetic suppression of calbindin-D28k.
Relatives of patients who have ALS are more likely to live with neuropsychiatric diseases such as schizophrenia, obsessive-compulsive disorder, and alcoholism.
Intestinal flora helps fight infection, inflammation, and cancer. What could this mean for neurodegeneration?
TREM2 accelerates neurodegeneration in one tauopathy model, but reduces tau pathology in another. Whether the microglial protein is good or bad may depend on stage of disease.
New CRISPR screen flags dozens of genes that suppress toxicity of the Parkinson’s protein. Tweaking multiple genes strengthened the protection.
Using modified MRI protocols, researchers were able to visualize these vessels in the dura mater of living people. The discovery challenges conventional wisdom.
Researchers claim this failed drug allows Aβ to accumulate inside cells, while small peptides cleaved from the C-terminal end of APP become trapped in membranes.
Human endothelial cells, smooth muscle cells, and astrocytes combine to form a vessel that ferries away Aβ, particularly Aβ42.
PET scans show a tangle patch in the entorhinal cortex when people report subjective cognitive concerns.
Young tau knockout mice maintain healthy brain tissue after ischemia, while older knockouts lose this stroke protection due to brain iron buildup.
Three developers of cryo-electron microscopy—the technique researchers recently used to unveil atomic structures of γ-secretase, Aβ, and tau fibrils—won this year’s Nobel Prize in chemistry.
The RNA-binding protein FUS promotes synthesis of an isoform of SynGAP, a protein that bolsters dendritic spines. Restoring SynGAP expression partially rescued deficits in FUS–deficient mice.
Seizures are a feature of AD, and are linked to cognitive decline. A new study reveals that, in mouse models of the disease, seizures induce the long-lasting transcription factor ΔFosB, which causes epigenetic suppression of the gene for calbindin-D28K, and memory deficits. Inhibiting ΔFosB or replacing calbindin-D28K improves memory in the mice.
With the recent discovery of lymph vessels in the human brain, never mind the glymphatic and perivascular drainage systems, does anybody truly understand how waste proteins leave the aging brain? And what do pericytes do, exactly? On Monday, October 30, leading international experts on protein clearance in neurodegenerative disease will discuss these questions and more during a daylong conference organized by UCL’s Leonard Wolfson Experimental Neurology Centre in London (see program). The meeting is sold out, but anyone can watch it on the UCLTV You Tube Channel, while joining a twitter debate via #UCLDementiaSeminars.
Genes work together, but most genetic screens assay them one at a time. A new CRISPR-based screen randomly disrupts the expression of many genes simultaneously. Researchers used the technique to identify dozens of genes that suppress toxicity of the Parkinson’s protein α-synuclein.
The long-standing dogma that the brain has no lymphatic system has fallen. Recent studies revealed lymphatic drainage from the brain in mice, and now a modified MRI protocol has visualized a similar network of vessels in the dura mater of human brains. While it remains to be shown how the system affects the clearance of brain waste such as Aβ, the finding changes fundamental assumptions about communication between the brain and the immune system.
Developed to reduce Aβ in the brain, the small-molecule drug semagacestat failed spectacularly in clinical trials when it worsened dementia in some cases. A new study claims that the drug allows Aβ and related peptides to accumulate intracellularly. The authors suggest semagacestat alters a previously unknown function of γ-secretase—translocation of Aβ across cell membranes—and they caution against using secreted Aβ as a measure of enzyme activity. But the data leave some key questions unresolved.
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- Michael Sasner on Microbiota from Wild Mice Protect Lab Mice from Disease
- Malu G. Tansey, Madelyn Houser and Andrew Neish on Microbiota from Wild Mice Protect Lab Mice from Disease
- Amy Nelson, Axel Montagne, Kassandra Kisler and Berislav Zlokovic on Lymphatic Vessels Found in Human Brain
- Roxana Carare and Roy Weller on Lymphatic Vessels Found in Human Brain
- Edward Blonz on ApoE4 Traps Insulin Receptor Inside Neurons
- Marcia Ratner on Tau Toxicity Blamed for Widespread Cell Death After Stroke
- Harald Steiner on Semagacestat, a Pseudo γ-Secretase Inhibitor?
- Roxana Carare and Roy Weller on Artificial Human Blood Vessels: A Model for Cerebral Amyloid Angiopathy?
- Igor Kurochkin on Semagacestat, a Pseudo γ-Secretase Inhibitor?
- Lili Zhang on Semagacestat, a Pseudo γ-Secretase Inhibitor?
- Erik Portelius on Semagacestat, a Pseudo γ-Secretase Inhibitor?
- Bart De Strooper on Semagacestat, a Pseudo γ-Secretase Inhibitor?
- Markus Zweckstetter on Cryo-EM Developers Win Nobel Prize in Chemistry
- Christoph Laske on Subjective Memory Complaints Tied to Tau
- Harald Hampel on Subjective Memory Complaints Tied to Tau
- Jeffrey L. Noebels on Tau Toxicity Blamed for Widespread Cell Death After Stroke
- Jean-Pierre Brion on Tau Toxicity Blamed for Widespread Cell Death After Stroke
- Seth Masters on New AD Target: Silencing the NLRP3 Inflammasome with Boron?
- Lewis H. Kuller on High Blood Pressure in Younger Adults: Dementia Risk Only in Women?
- Boon-Seng Wong on ApoE4 Traps Insulin Receptor Inside Neurons