Silvia Zampar

ORCID: 0000-0003-0134-0974
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Computational Drug Discovery Methods
  • Tryptophan and brain disorders
  • Nuclear Receptors and Signaling
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Adipose Tissue and Metabolism
  • Neuroendocrine regulation and behavior
  • Stress Responses and Cortisol
  • Prion Diseases and Protein Misfolding
  • Genetic Neurodegenerative Diseases
  • Diet and metabolism studies
  • Genetic Associations and Epidemiology
  • RNA Research and Splicing
  • Macrophage Migration Inhibitory Factor
  • RNA regulation and disease
  • GDF15 and Related Biomarkers
  • Genetics and Neurodevelopmental Disorders
  • interferon and immune responses

Ontario Brain Institute
2024

University Health Network
2024

Occupational Cancer Research Centre
2024

University of Toronto
2024

University of Göttingen
2018-2023

Universitätsmedizin Göttingen
2021-2022

University of Milan
2019-2020

The incidence of Alzheimer's disease (AD), the leading cause dementia, increases rapidly with age, but why age constitutes main risk factor is still poorly understood. Brain ageing affects oligodendrocytes and structural integrity myelin sheaths1, latter which associated secondary neuroinflammation2,3. As support axonal energy metabolism neuronal health4-7, we hypothesized that loss could be an upstream for amyloid-β (Aβ) deposition, central neuropathological hallmark AD. Here identify...

10.1038/s41586-023-06120-6 article EN cc-by Nature 2023-05-31

Infantile-onset RNaseT2 deficient leukoencephalopathy is characterised by cystic brain lesions, multifocal white matter alterations, cerebral atrophy, and severe psychomotor impairment. The phenotype similar to congenital cytomegalovirus infection overlaps with type I interferonopathies, suggesting a role for innate immunity in its pathophysiology. To date, pathophysiological studies have been hindered the lack of mouse models recapitulating neuroinflammatory encephalopathy found patients....

10.1038/s41467-021-26880-x article EN cc-by Nature Communications 2021-11-11

Aims The deposition of amyloid‐β (Aβ) peptides in the form extracellular plaques brain represents one classical hallmarks Alzheimer’s disease (AD). In addition to ‘full‐length’ Aβ starting with aspartic acid (Asp‐1), considerable amounts various shorter, N‐terminally truncated have been identified by mass spectrometry autopsy samples from individuals AD. Methods Selectivity several antibodies detecting full‐length, total or species has characterized capillary isoelectric focusing assays...

10.1111/nan.12637 article EN cc-by-nc Neuropathology and Applied Neurobiology 2020-06-04

The prevalence of Alzheimer’s disease (AD), the leading cause dementia, shows a strict age-dependency, but why ageing constitutes main risk factor for this is still poorly understood. Brain affects oligodendrocytes 1 and structural integrity myelin sheaths 2 , latter associated with secondary neuroinflammation 3 . Since support axonal neuronal health 4–7 we hypothesised that ageing-associated loss could be an upstream amyloid-β (Aβ) deposition, primary neuropathological hallmark AD. Here,...

10.1101/2021.07.31.454562 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-08-02

Abstract β-Site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is the major described β-secretase to generate Aβ peptides in Alzheimer’s disease (AD). However, all therapeutic attempts block BACE1 activity and improve AD symptoms have so far failed. A potential candidate for alternative generation metalloproteinase meprin β, which cleaves APP predominantly at alanine p2 this study we can detect an increased β expression brain. Here, report of transgenic APP/lon mouse model lacking...

10.1007/s00018-022-04205-5 article EN cc-by Cellular and Molecular Life Sciences 2022-03-01

A variety of factors has been associated with healthy brain aging, and epidemiological studies suggest that physical activity nutritional supplements such as caffeine may reduce the risk developing dementia and, in particular, Alzheimer’s disease (AD) later life. Caffeine is known to act a cognitive enhancer but also shown positively affect exercise performance endurance activities. We have previously observed chronic oral supplementation treatment paradigm encompassing stimulation by...

10.3390/ijms24032155 article EN International Journal of Molecular Sciences 2023-01-21

The ratio of amyloid precursor protein (APP)669–711 (Aβ−3–40)/Aβ1–42 in blood plasma was reported to represent a novel Alzheimer’s disease biomarker. Here, we describe the characterization two antibodies against N-terminus Aβ−3–x and development “fit-for-purpose” technical validation sandwich immunoassay for measurement Aβ−3–40. Antibody selectivity assessed by capillary isoelectric focusing immunoassay, Western blot analysis, immunohistochemistry. analytical addressed assay range,...

10.3390/ijms21186564 article EN International Journal of Molecular Sciences 2020-09-08

There is growing evidence from epidemiological studies that especially midlife physical activity might exert a positive influence on the risk and progression of Alzheimer’s disease. In this study, Tg4-42 mouse model disease has been utilized to assess effect different housing conditions structural changes in hippocampus. Focusing dentate gyrus, we demonstrate 6-month-old mice have reduced number newborn neurons comparison age-matched wild-type mice. Housing these for 4 months with either...

10.1177/1759091419892692 article EN cc-by-nc ASN NEURO 2019-01-01

In sporadic Alzheimer's disease (AD), an imbalance between production and clearance of amyloid-β (Aβ) peptides seems to account for enhanced Aβ accumulation. The metalloprotease neprilysin (NEP) is important degrading enzyme as shown by a variety in vitro vivo studies. While the deg radation full-length such Aβ1-40 Aβ1-42 well established, it less clear whether NEP also capable N-terminally truncated species common variant Aβ4-42. present report, we confirmed degradation Aβ4-x using...

10.3233/jad-181134 article EN Journal of Alzheimer s Disease 2019-01-18

The relationship between the two most prominent neuropathological hallmarks of Alzheimer’s Disease (AD), extracellular amyloid-β (Aβ) deposits and intracellular accumulation hyperphosphorylated tau in neurofibrillary tangles (NFT), remains at present not fully understood. A large body evidence places Aβ upstream cascade pathological events, triggering NFTs formation subsequent neuron loss. Extracellular were indeed causative an increased phosphorylation several transgenic models but...

10.3390/ijms22105191 article EN International Journal of Molecular Sciences 2021-05-14

Regular physical activity has been associated with healthy brain aging, reflected by beneficial effects on cognition and learning memory. Nutritional supplements such as caffeine have shown to act cognitive enhancers may possess neuroprotective properties. Interestingly, also improves athletic capabilities is widely used athletes because of its performance-enhancing effect, while information potential additive performance scarce. In the present study, supplementation in combination prolonged...

10.1007/s00406-022-01431-7 article EN cc-by European Archives of Psychiatry and Clinical Neuroscience 2022-06-09
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