Publications by authors named "Anna Mengr"

Alzheimer's disease (AD) is the most common form of dementia. Characterized by progressive neurodegeneration, AD typically begins with mild cognitive decline escalating to severe impairment in communication and responsiveness. It primarily affects cerebral regions responsible for cognition, memory, and language processing, significantly impeding the functional independence of patients.

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Cholesterol plays an important biological role in the body, and its disruption in homeostasis and synthesis has been implicated in several diseases. Mapping the locations of cholesterol is crucial for gaining a better understanding of these conditions. Silver deposition has proven to be an effective method for analyzing cholesterol using mass spectrometry imaging (MSI).

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Alzheimer's disease (AD) is a progressive brain disorder characterized by extracellular amyloid-β (Aβ) plaques, intracellular neurofibrillary tangles formed by hyperphosphorylated Tau protein and neuroinflammation. Previous research has shown that obesity and type 2 diabetes mellitus, underlined by insulin resistance (IR), are risk factors for neurodegenerative disorders. In this study, obesity-induced peripheral and central IR and inflammation were studied in relation to AD-like pathology in the brains and periphery of APP/PS1 mice, a model of Aβ pathology, fed a high-fat diet (HFD).

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Obesity and type 2 diabetes mellitus (T2DM) are preconditions for the development of metabolic syndrome, which is reaching pandemic levels worldwide, but there are still only a few anti-obesity drugs available. One of the promising tools for the treatment of obesity and related metabolic complications is anorexigenic peptides, such as prolactin-releasing peptide (PrRP). PrRP is a centrally acting neuropeptide involved in food intake and body weight (BW) regulation.

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Article Synopsis
  • Prolactin-releasing peptide (PrRP) analog palm11-PrRP31 shows potential in treating obesity and Type 2 Diabetes, and has been found to reduce Alzheimer-related Aβ plaque load and inflammation in APP/PS1 mice.
  • The study investigated the effects of palm11-PrRP31 on neuroprotection and synaptogenesis in the cerebellum, given that Aβ plaques may contribute to cognitive deficits in Alzheimer's Disease.
  • Results indicated that palm11-PrRP31 treatment reduced Aβ plaques and microgliosis, while also promoting synaptogenesis and reducing neuroinflammation and apoptosis in the hippocampus, highlighting its potential in neurodegenerative disorder treatment.
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