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.
The first large-scale surveys of DNA methylation in Alzheimer’s brains turned up numerous altered regions that may point to new genes involved in pathology.
Researchers predict that a new BACE1 mouse recapitulates the early stages of sporadic Alzheimer’s, and can serve as a testing ground for BACE1 inhibitors.
Compounds that bind RNA temper toxicity related to ALS and FTD.
Connections across neural networks break down as cognition declines in people with different forms of AD, suggesting the wiring problems may be a hallmark of disease progression.
Researchers are ramping up efforts to target tau for Alzheimer’s and other tauopathies.
Blocking the microglial receptor for pro-inflammatory prostaglandin D2 protects motor neurons from glial toxicity in ALS cell and mouse models.
After numerous disappointing trials of Alzheimer therapies that tackle Aβ, researchers are developing ways of targeting the peptide’s partner in crime, i.e., tau. As Alzforum wraps up coverage of the Alzheimer’s Association International Conference 2014, held July 12-17 in Copenhagen, Denmark, read how scientists are harnessing immunotherapy and anti-aggregation schemes to try to rid the body of the other pathological hallmark of AD.
- Daniel Michaelson on Effects of the Absence of Apolipoprotein E on Lipoproteins, Neurocognitive Function, and Retinal Function.
- Gary Landreth on Effects of the Absence of Apolipoprotein E on Lipoproteins, Neurocognitive Function, and Retinal Function.
- Leon Tai, Manel Ben Aissa and Mary Jo LaDu on ApoE: One Man’s Brain Can Do Without It
- Suzana Petanceska on Alzheimer’s Brains Mottled with Epigenetic Changes
- Samantha Budd on Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes.
- Stefan Lichtenthaler on Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes.
- Frank LaFerla on Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes.