Transcranial magnetic stimulation of the parietal cortex strengthens a hippocampal network involved in associative memory and transiently improves memory performance.
Improved magnetic resonance imaging methods confirm damage in a subclass of motor neurons in ALS.
In a reverse twist on the spread of pathology in Alzheimer’s, axonal proteins translated in the presence of Aβ migrate back to cell bodies, where they promote cell death.
Aβ in mitochondria slows the maturation of proteins that enter the organelle from cytosol, according to a new study. The finding could help explain the wide range of mitochondrial deficits seen in Alzheimer’s disease.
Restraining the activity of a calcium-activated phosphatase may take the edge off a-synuclein toxicity.
According to new research, as both mice and humans grow older, immune signals change at the interface between blood and cerebrospinal fluid.
Perfectly healthy mitochondria can sicken neurons simply by being in the wrong place.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
Clinicians use transcranial magnetic stimulation to lift depression, but what else could this technique do? In the August 29 Science, researchers report that stimulating a hippocampal brain network with a wire coil held to the outside of the head temporarily enhances associative memory in healthy young volunteers. The findings provide a way to bolster a specific cognitive ability without drugs or surgery, although much more work remains to determine if this approach could help older people with memory disorders.
Researchers have uncovered a single mechanism that could explain how Aβ manages to derail a multitude of mitochondrial functions. The peptide, which is known to build up in these organelles, inhibits the maturation of proteins imported from the cytosol. According to the research, Aβ indirectly interferes with the removal of N-terminal mitochondrial localization sequences. Without proper trimming, these crucial protein immigrants destabilize and compromise the mitochondria. The findings further implicate the cell’s powerhouses in AD pathology.
- John Kane and Mary Malloy on ApoE: One Man’s Brain Can Do Without It
- Xiongwei Zhu on Amyloid-β Peptide Induces Mitochondrial Dysfunction by Inhibition of Preprotein Maturation.
- M Flint Beal on Amyloid-β Peptide Induces Mitochondrial Dysfunction by Inhibition of Preprotein Maturation.
- Russell Swerdlow on Amyloid-β Peptide Induces Mitochondrial Dysfunction by Inhibition of Preprotein Maturation.
- Bettina Platt on PLB4 (hBACE1)
- Masato Mitsuhashi on Exosomes Stand Out as Potential Blood Biomarkers
- Daniel Michaelson on Effects of the Absence of Apolipoprotein E on Lipoproteins, Neurocognitive Function, and Retinal Function.