At Tau2022: Unknown Functions Emerge for Tau, LRRK2
Neurons need LRRK2 in order to take up tau from the extracellular milieu. In ALS neurons, tau scuppers mitochondria, whereas in healthy cells it helps the nucleolus to function correctly.
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Neurons need LRRK2 in order to take up tau from the extracellular milieu. In ALS neurons, tau scuppers mitochondria, whereas in healthy cells it helps the nucleolus to function correctly.
Limbic TDP-43 pathology accelerates cognitive decline in people with or without AD. Exosome and imaging biomarkers look promising.
Once p-tau217 in cerebrospinal fluid reaches a tipping point, it rises at a constant rate in everyone and predicts the age when symptoms will begin.
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.
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
The data, from mice, help explain how these depressants may increase a person’s risk for dementia.
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.
Retarding glymphatic clearance in mice caused p-tau to accumulate faster, and hastened neurodegeneration.
The comment period ends with nearly 10,000 submissions split between pro and con, letter-writing campaigns, and scrutiny from U.S. Congress. Even so, scientists say, not much has changed.
Heterogenous oligomers that include shorter Aβ peptides, such as Aβ37 and Aβ38, along with Aβ42 do not form fibrils, slowing plaque growth.
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
In a career that spanned more than 40 years, Trojanowski broadened and deepened the field's understanding of the molecular pathology of neurodegenerative diseases.
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
Large multinational meta-analysis also found that among people without dementia, CSF Aβ42 edged out PET in detecting amyloid pathology.