Publications by authors named "Anna M Lilja"

Article Synopsis
  • Amyloid-β immunotherapy is gaining attention as a potential treatment for Alzheimer's disease, with several monoclonal antibodies in clinical trials; two are in phase 3, and one has already been FDA approved.
  • The focus of the research is on creating an enhanced hexavalent antibody based on mAb158, which targets toxic Aβ protofibrils, and evaluating its binding properties and protective capabilities against Aβ-induced cell damage.
  • Results show that the hexavalent antibody design significantly improves binding to protofibrils (40 times more effective) and effectively interacts with various Aβ aggregates, demonstrating potential as a therapeutic option for Alzheimer's disease.
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Recent lineage tracing studies have revealed that mammary gland homeostasis relies on unipotent stem cells. However, whether and when lineage restriction occurs during embryonic mammary development, and which signals orchestrate cell fate specification, remain unknown. Using a combination of in vivo clonal analysis with whole mount immunofluorescence and mathematical modelling of clonal dynamics, we found that embryonic multipotent mammary cells become lineage-restricted surprisingly early in development, with evidence for unipotency as early as E12.

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Ensuring that pregnant women are delivering in a health facility and are attended to by skilled birth attendants is critical to reducing maternal and infant morbidity and mortality. This study sought to determine the associations between male involvement in antenatal care (ANC) services and pregnant women delivering at health facilities and being attended to by skilled birth attendants as well as attending postnatal care. This was a retrospective cohort study using secondary analysis of program data.

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Stimulating regeneration in the brain has the potential to rescue neuronal networks and counteract progressive pathological changes in Alzheimer's disease (AD). This study investigated whether drugs with different mechanisms of action could enhance neurogenesis and improve cognition in mice receiving human neural stem cell (hNSC) transplants. Six- to nine-month-old AD Tg2576 mice were treated for five weeks with the amyloid-modulatory and neurotrophic drug (+)-phenserine or with the partial α7 nicotinic receptor (nAChR) agonist JN403, combined with bilateral intrahippocampal hNSC transplantation.

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The objective of this study was to investigate the effects of modulating brain amyloid-β (Aβ) levels at different stages of amyloid pathology on synaptic function, inflammatory cell changes and hippocampal neurogenesis, i.e. processes perturbed in Alzheimer's disease (AD).

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Neuronal dysfunction and demise together with a reduction in neurogenesis are cardinal features of Alzheimer's disease (AD) induced by a combination of oxidative stress, toxic amyloid-β peptide (Aβ) and a loss of trophic factor support. Amelioration of these was assessed with the Aβ lowering AD experimental drugs (+)-phenserine and (-)-phenserine in neuronal cultures, and actions in mice were evaluated with (+)-phenserine. Both experimental drugs together with the metabolite N1-norphenserine induced neurotrophic actions in human SH-SY5Y cells that were mediated by the protein kinase C (PKC) and extracellular signal-regulated kinases (ERK) pathways, were evident in cells expressing amyloid precursor protein Swedish mutation (APP(SWE)), and retained in the presence of Aβ and oxidative stress challenge.

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Amyloid-β (Aβ) peptides in the brain of patients with Alzheimer's disease (AD) assemble into various aggregation forms that differ in size, structure, and functional properties. Previous studies have shown that Aβ binds to nicotinic acetylcholine receptors (nAChRs) and activates signaling cascades that result in the disruption of synaptic functions. These findings suggest a possible link between impaired cholinergic neurotransmitter function in AD and Aβ pathogenesis.

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