Publications by authors named "W P Spencer"

Supporting older people to age well is a global policy priority, however the development and implementation of strategies to support ageing well for older Aboriginal people must be determined by the communities affected. This is necessary in colonial contexts, where socio-political structures impinge on Aboriginal rights and mainstream policy and practice creates and maintains health and social inequities. This article reports on research conducted in partnership with the Dharriwaa Elders Group, an Aboriginal Community Controlled Organisation.

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In humans, inositol polyphosphate-5-phosphatase e (INPP5E) mutations cause retinal degeneration as part of Joubert and MORM syndromes and can also cause non-syndromic blindness. In mice, mutations cause a spectrum of brain, kidney, and other anomalies and prevent the formation of photoreceptor outer segments. To further explore the function of Inpp5e in photoreceptors, we generated conditional and inducible knockouts of mouse Inpp5e where the gene was deleted either during outer segment formation or after outer segments were fully formed.

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Objective: To measure current levels and experiences of food and water security in Walgett to guide a community-led program and to provide a baseline measure.

Design: A community-led cross-sectional survey conducted in April 2022 by trained local researchers.

Setting: Walgett, a regional town in NSW, Australia.

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Pathogenic coding mutations are prevalent in human neuronal transcription factors (TFs) but how they disrupt development is poorly understood. Lmx1b is a master transcriptional regulator of postmitotic neurons that give rise to mature serotonin (5-HT) neurons; over two hundred pathogenic heterozygous mutations have been discovered in human yet their impact on brain development has not been investigated. Here, we developed mouse models with different DNA-binding missense mutations.

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Article Synopsis
  • Age-related macular degeneration (AMD) and related macular dystrophies (MDs) primarily impact the retinal pigment epithelium (RPE) with drusen deposits being a key feature in the progression of these diseases.
  • The research indicates that reduced activity of matrix metalloproteinase 2 (MMP2) in RPE contributes to drusen formation by causing sterile inflammation and disrupting lipid balance, interacting with specific receptors and molecules.
  • Therapeutic approaches including MMP2 supplementation and inhibiting RAGE and sPLA2-IIA have shown promise in reducing drusen accumulation in patient-derived RPE cells, highlighting a potential treatment pathway for AMD/MDs.
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