Compound clears Phase 1 hurdle.
A drug that inhibits the sodium/potassium pump rescues a mouse model of the disease.
A protease previously linked to hyperphosphorylation of tau is now found to cleave the protein. The enzyme worsens tau pathology in transgenic mice.
A small Aβ fragment produced in healthy brains binds acetylcholine receptors and enhances synaptic plasticity and learning, while blocking the toxic effects of Aβ42.
Compounds derived from cocoa beans boost blood volume to part of the brain, and may counteract age-related decline in memory.
A broad genetic analysis suggests that mutations in a microtubule subunit enhance the risk for ALS.
A protein from the Borna disease virus rescues mitochondria and keeps stressed neurons viable, suggesting a new neuroprotective strategy.
MRI in mice could help explain disconnections in neural circuitry that precede amyloid plaques.
Scientists have uncovered another clue to the pathology that drives amyotrophic lateral sclerosis. New research suggests that when astrocytes overproduce a sodium-potassium pump, nearby neurons take a hit. Digoxin, a compound that blocks a similar pump in heart muscle, protected mice that model the motor neuron disease. Though digoxin poorly penetrates the central nervous system, a similar treatment might work for ALS, suggest the researchers.
Aβ fragments are not always bad guys. Researchers in Hawaii recently identified one that boosts synaptic plasticity and learning. Aβ15, which corresponds to the N-terminal portion of Aβ42, also blocked the toxic effects of the larger fragment in vitro.
Finding genetic variations that cause extremely rare conditions, such as amyotrophic lateral sclerosis, presents scientists with a major challenge. Now, using a novel, exome-based approach, an international group of researchers has turned up a potential risk factor for ALS in the TUBA4A gene, which codes for an isoform of α-tubulin. TUBA4A variants that associate with ALS weaken the microtubules that form the cytoskeleton, according to the research. The findings may help explain why neurons degenerate in this disease.
Not all viruses kill their prey. In fact, at least one virus that invades neurons preserves its hosts by turning off cell death pathways. Now, researchers have used this trick to stave off neurodegeneration. In Nature Communications, French researchers report that a protein from the Borna disease virus protects mitochondria and rescues neurons in a mouse model of Parkinson’s. A fragment of the protein may work as a neuroprotective agent.
At the 139th meeting of the American Neurological Association, held October 12-14 in Baltimore, scientists explained some of the newest therapies, preventative techniques, and diagnostic tests that may help control Alzheimer’s disease. An in vitro fertilization procedure has helped one woman who has early-onset Alzheimer’s in her family conceive twins with normal copies of the presenilin 1 gene. On the therapeutics front, a drug that is FDA-approved to quell uncontrollable laughing and crying reduced emotional outbursts and calmed patients with Alzheimer’s and other dementias. In addition, scientists reported that Raman spectroscopy of the blood might distinguish people with AD from healthy peers and people with other dementias.
- Kelly Dakin on SIRT1 suppresses beta-amyloid production by activating the alpha-secretase gene ADAM10.
- Ruth Itzhaki on A Kinder Pathogen? Viral Protein Preserves Neurons in Parkinson’s Model
- Christian Lobsiger on An α2-Na/K ATPase/α-adducin complex in astrocytes triggers non-cell autonomous neurodegeneration.
- Albrecht Clement on An α2-Na/K ATPase/α-adducin complex in astrocytes triggers non-cell autonomous neurodegeneration.
- Richard Bedlack on An α2-Na/K ATPase/α-adducin complex in astrocytes triggers non-cell autonomous neurodegeneration.
- Erik Portelius on Cleavage of tau by asparagine endopeptidase mediates the neurofibrillary pathology in Alzheimer's disease.
- John Cirrito on Regulation of Presynaptic Ca2+, Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal β-Amyloid Fragment.