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.
Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.
Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.