Wolframin-1 Cells: Tau’s Launch Pad from Entorhinal Cortex to Hippocampus?
Misfolded tau travels from a subset of neurons in the entorhinal cortex directly into CA1 neurons in the hippocampus, fouling synaptic transmission and memory in mice.
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Misfolded tau travels from a subset of neurons in the entorhinal cortex directly into CA1 neurons in the hippocampus, fouling synaptic transmission and memory in mice.
The academy elected 90 new members. Five are well-known for their contributions to the field of neurodegenerative diseases.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.
In Alzheimer's mice without the AD risk gene Abi3, fewer microglia crowd around amyloid plaques. Cultured microglia without Abi3 appear stuck in a torpor, even though their phagocytosis mostly works.
The new gene JADE1 encodes an adaptor protein that sits in tangles and nonetheless appears neuroprotective. The study also turned up three AD and two PSP genes, suggesting PART overlaps with these conditions.
In a mouse model of amyloidosis, microglia carried Aβ aggregates into grafted wild-type tissue. The immune cells played a key part in the subsequent growth of plaques in the graft.
While Phase 3 trials of subcutaneous gantenerumab continue, scientists say delivering the antibody to the brain via the transferrin receptor might be twice as efficient.
Blood from fit mice reduced neuroinflammation in inactive mice. The can-do component? Clusterin, an apolipoprotein linked to Alzheimer’s. Clusterin tamped down interferon and cytokine signaling.
The EMA's decision was expected. Biogen announced it will appeal but also halved the drug's price. The company said it plans to complete a confirmatory trial by 2026.
Tissues from old people, both healthy and diseased, overexpress genes lacking C-G repeats. This stokes inflammation, possibly explaining why neurodegeneration rises with age.
Alzforum editors review the highlights of last year’s clinical and research developments.
While payers public and private are deliberating whether or not to cover this first-in-class drug, the health economics group ICER re-affirms its original conclusion that aducanumab is overpriced.
The compound had shown promise for sharpening cognition in schizophrenia and Alzheimer’s, but now faces an uncertain future.
Virtual Workshop Tackles LATE, a Cause of Late-life Dementia Scientists Say LATE Worsens Cognitive Decline Does LATE Subvert Alzheimer's Trials? Biomarkers, Please! LATE (Limbic-predominant Age-related TDP-43 Encephalopathy) 2022
Limbic predominant age-related TDP-43 encephalopathy is strikingly common among octo- and nonagenarians, and it causes their cognition to slide. LATE dramatically boosts the risk of dementia among people who also have plaques and tangles.