The longevity-associated variant of BPIFB4 improves a CXCR4-mediated striatum–microglia crosstalk preventing disease progression in a mouse model of Huntington’s disease
Alba Di Pardo; Elena Ciaglia; Monica Cattaneo; Anna Maciąg; Francesco Montella; Valentina Lopardo; Anna Ferrario; Francesco Villa · 2020 · Cell Death and Disease
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Abstract The longevity-associated variant (LAV) of the bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) has been found significantly enriched in long-living individuals. Neuroinflammation is a key player in Huntington’s disease (HD), a neurodegenerative disorder caused by neural death due to expanded CAG repeats encoding a long polyglutamine tract in the huntingtin protein (Htt). Herein, we showed that striatal-derived cell lines with expanded Htt (STHdh Q 111/111 ) expressed and secreted lower levels of BPIFB4, when compared with Htt expressing cells (STHdh Q 7/
Abstract by Alba Di Pardo; Elena Ciaglia; Monica Cattaneo; Anna Maciąg; Francesco Montella; Valentina Lopardo; Anna Ferrario; Francesco Villa, Cell Death and Disease (2020) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1038/s41419-020-02754-w