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At LATE 2022, researchers hashed out neuropathological and clinical characteristics of limbic predominant age-related TDP-43 encephalopathy, a major contributor to late-life cognitive decline and potential bungler of AD clinical trials.
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
Single-nuclei expression analysis identified different cell clusters from people who carried autosomal-dominant Alzheimer’s mutations or risk variants for late-onset AD. Also, microglia RNA-Seq goes big.
Shrinkage of distinct brain regions in the frontal and temporal lobes may unsuppress neural activity in the dorsal stream, a region involved in visual perception.
New research reveals fundamental roles for astrocytes and microglia in shaping neural circuits.
The U.S. Food and Drug Administration will convene an advisory committee to guide its decision, which will affect how widely available the treatment will be.
Carriers of R145C were more likely to get AD, but only if they co-inherited a copy of ApoE4.
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...
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