As data increasingly blame the microglia response as a driving force in Alzheimer’s disease, researchers are investigating whether tempering these cells will aid cognition.
An FDA-approved insomnia drug lengthened total sleep time in patients with mild to moderate Alzheimer’s, suggesting it might be able to lessen a troublesome symptom of the disease.
In the largest study yet to track tau via repeated PET scans, researchers found that tau pathology increased over baseline only in people with Aβ deposition. The more tau a person had at baseline, the more tau increased later on, and the more they slipped on cognitive tests.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
In ADNI, blood marker exposes ongoing neurodegeneration across disease stages.
Scientists propose that LATE is a neurodegenerative disease marked by TDP-43 pathology in limbic regions, and memory loss. After death, it can be seen alone or with other pathology.
Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.
Scientists are probing saliva and skin secretions for telltale signs of Parkinson’s disease. Their prize? A diagnostic test at the pre-motor stage.
By slipping human microglia inside the mouse brain, researchers hope to better monitor their response to pathologies, such as Aβ.
People who take leisurely walks, garden, and tackle household chores had bigger brains than those who were more sedentary. Vigorous exercise brought neither additional benefit nor harm.
Diagnostics Accelerator to fund projects that develop dementia biomarkers from patient data.
Long-term treatment with the anti-sense oligonucleotide led to motor benefits in an extension trial of children 2 to 15 years old.
Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.