Molecular Structure of LRRK2 Gives Clues to Parkinson’s
The first high-resolution look at LRRK2 implies that pathogenic mutations increase binding to microtubules by biasing the kinase domain toward a closed, active conformation.
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The first high-resolution look at LRRK2 implies that pathogenic mutations increase binding to microtubules by biasing the kinase domain toward a closed, active conformation.
A C9ORF72 polydipeptide repeat induces aggregation by direct interaction with TDP-43, while progranulin mutations that trigger microglial toxicity cause TDP-43 to accumulate via complement.
While one anti-Aβ antibody thwarts initial seeding of fibrils, and others keep fibrils from lengthening, aducanumab prevents oligomers forming on their surface. In vitro, that is.
In mice, accumulation of tau in hilar astrocytes of the dentate gyrus spells trouble for the hippocampus and for spatial memory.
The brain shrinkage due to verubecestat emerged quickly but did not worsen or cause neurodegeneration. Curiously, both verubecestat and lanabecestat dulled episodic memory and boosted verbal fluency.
Researchers identified genetic variants that may explain why some ApoE4 carriers remain free of Alzheimer’s, while some ApoE2 carriers do not.
The first ultrasensitive plasma test for this old marker differentiates Alzheimer’s from healthy controls and non-AD dementias. It segregates people stepwise at phases of pathogenesis down to Braak stages 1 and 2 and below amyloid PET positivity.
Van Leeuwen was best known for finding frameshift mutations in APP and ubiquitin B in the brains of people with tauopathies.
Both shy and funny, Allsop was a pioneer of modern Alzheimer's research.
African Americans are likelier than non-Hispanic Caucasians to carry low-expression TREM2 variants, and less likely to carry a high-expression variant. As a result, they have less soluble TREM2 in their cerebrospinal fluid.
People who develop Type 2 diabetes before age 60 have more than double the dementia risk, and earlier dementia onset, than those without diabetes.
The fewer their meningeal lymphatic vessels, the slower treated mice clear plaques. Lymphatic dysfunction also drives microglial activation, hinting at a role in pathology.
A “mammalian-wide interspersed repeat-natural antisense transcript” blocks translation of tau mRNA. Other MIR-NATS may act on α-synuclein and APP.
Via recently discovered channels, freshly made monocytes and B cells in the bone marrow of the skull and vertebrae travel directly into the meninges, where they stand ready to infiltrate the brain. These immune cells are distinct from their blood-borne counterparts.
In a tauopathy mouse model, overexpressing the receptor lowered ApoE, prevented microglial activation, and lessened neurodegeneration. LDLR—a drug target for neuroprotection?
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