Can Induced Neurons Identify Early Signs of Neurodegeneration?
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
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In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
Using different approaches, two recent animal studies have reported some success toward achieving a goal common to several experimental AD therapies: Both methods significantly lowered the Aβ burden in the brain...
In “Maintain Your Brain,” virtual interventions gave participants a memory boost. In EXERT, cognition held steady in people who exercised. Both groups were coached.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
As FTD consortia chase biomarkers, they see plasma NfL and neuronal pentraxin-2—which reflect neurodegeneration—change before symptoms. Trials nudge progranulin and poly-DP. Still needed: more markers of the pathophysiology that unfolds in the brain.
At Keystone, researchers placed pathological tau on both sides of the synaptic cleft, along with complement proteins. Activated microglia gobbled up tau-laden neurons, and even may have facilitated tau’s spread in the brain.
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
The rarest kind of Alzheimer disease (AD)—the autosomal-dominant form that runs in families—has long been marked by its untapped opportunities...
Inclusions in tau seed sensor cells are made of amyloid fibrils, say scientists at AD/PD 2023. In those cells, and in human neurons, a dis-aggregase shreds them.
Biogen/IONIS’s tau ASO BIIB080 dropped participants’ tau PET signal below baseline in six months of treatment, according to data from a Phase 1 study presented at AD/PD.
Perivascular macrophages both produce and react to the apolipoprotein, releasing toxic reactive oxygen species that constrict blood vessels.
While a death causes jitters, new blood phospho-tau data from Phase 3 trials strengthen the antibody’s claim to disease modification, and post-market studies seek evidence of benefit.
At AD/PD, scientists showed 3- and 4-year amyloid immunotherapy data hinting at sustained cognitive benefits. The number of remaining participants is tiny.
The microglial receptor activates an antiviral signaling cascade. The virus downregulates TREM2 expression after infecting microglia.
In a head-to-head comparison, donanemab banished four times as much plaque in the first six months as aducanumab did, partly due to its faster titration.