Using microglia and an unbiased screening method, investigators have identified almost 60 previously unknown targets for γ-secretase. Investigators from KU Leuven and colleagues published their results in Molecular Cell on Nov. 16, 2023.
The advent of FDA-approved therapies for Alzheimer’s disease has had some downstream regulatory effects, including that the Centers for Medicare & Medicaid Services recently announced it will eliminate the coverage with evidence development (CED) requirement for PET imaging for beta amyloid imaging for Alzheimer's disease.
By creating a new mouse model of Alzheimer’s disease that better recapitulated how the disease plays out in humans, investigators at KU Leuven have gained new insights into how amyloid plaques, tau tangles and neuronal death are related at the molecular level.
Investigators have identified a second individual who remained cognitively normal into his late 60s despite having the PSEN1 E280A mutation, which causes a familial version of early-onset Alzheimer’s disease (AD). The likely source of protection, a mutation in a gene called Reelin, is distinct from the protective mechanism identified in the first case of an individual who was protected from the effects of PSEN1 E280A. That case was reported in 2019.
The aqueous supernatants resulting from ultracentrifugation of brain samples from patients with Alzheimer’s disease (AD) contain aggregates so far described as soluble oligomers of amyloid-β protein (Aβ), which are responsible for the neurotoxicity underlying AD and thus considered targets to watch in this devastating condition. Now, a group of scientists from Harvard Medical School have determined that these aggregates are in fact insoluble diffusible fibrils with the same atomic structure as plaque fibrils.
Researchers have identified a link between amyloid plaques and dysfunctional neuronal conduction in animal models of Alzheimer’s disease (AD). Their study, which was published in the Dec. 1, 2022, issue of Nature, suggests new ways to think about AD, as well as badly needed potential alternatives to plaque removal to fight the disease.
Researchers have identified a link between amyloid plaques and dysfunctional neuronal conduction in animal models of Alzheimer’s disease (AD). Their study, which was published in the Dec. 1, 2022, issue of Nature, suggests new ways to think about AD, as well as badly needed potential alternatives to plaque removal to fight the disease.
Researchers at the University of Cincinnati have published data showing that in patients with dominantly inherited Alzheimer’s disease-causing mutations, high levels of soluble amyloid-β42 (Aβ42) in the cerebrospinal fluid predicted a reduced risk of developing dementia over three years.
Investigators at the Weizmann Institute of Science have identified changes in oligodendrocytes that were shared across multiple dementia types. The team reported its results in the June 27, 2022, online issue of NatureNeuroscience.
