
Christiana BjorkliNorwegian University of Science and Technology | NTNU · Department of Neuromedicine and Movement Science
Christiana Bjorkli
PhD in Medicine
About
13
Publications
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Introduction
In my PhD project I aim to disentangle Alzheimer's disease (AD) by using rodent models, by answering four timely questions:
1) How well can we translate fluid biomarkers between AD models and patients?
2) Is it possible to longitudinally measure in vivo biochemical changes in AD biomarkers in models?
3) Are repurposed drugs effective in hindering AD neuropathology in models?
4) Can AD neuropathology spread be hindered when its cortical origin is manipulated?
Publications
Publications (13)
The central canal (CC) of the spinal cord is a neurogenic niche consisting of quiescent neural stem cells (NSCs) capable of responding to traumatic damage to the spinal cord by increasing their proliferative activity and sending migrating progeny toward the site of injury, where they contribute to the formation of the glial scar. However, CC NSCs h...
The subventricular zone (SVZ) of the lateral ventricle and subgranular zone (SGZ) of the dentate gyrus (DG) in the hippocampus represents neurogenic niches within the brain housing distinct populations of neural stem cells (NSCs), known for their exclusive capacity to sustain neurogenesis in the adult mammalian CNS. These niches respond to traumati...
Projection neurons in the anteriolateral part of entorhinal cortex layer II are the predominant cortical site for hyperphosphorylation of tau and formation of neurofibrillary tangles in prodromal Alzheimer’s disease. A majority of layer II projection-neurons in anteriolateral entorhinal cortex are unique among cortical excitatory neurons by express...
All drug trials completed to date have fallen short of meeting the clinical endpoint of significantly slowing cognitive decline in Alzheimer’s disease (AD) patients. In this study, we repurposed two FDA-approved drugs, Fasudil and Lonafarnib, targeting synaptic formation (i.e., Wnt signaling) and cellular clearance (i.e., autophagic) pathways respe...
One of the neuropathological hallmarks of Alzheimer’s disease (AD) is the accumulation of amyloid-β (Aβ) plaques, which is preceded by intraneuronal build-up of toxic, aggregated Aβ during disease progression. Aβ plaques are first deposited in the neocortex before appearing in the medial temporal lobe, and tau pathology with subsequent neurodegener...
Simplified Gallyas-silver staining protocol that works for pathological staining in rodent and human tissue
Projection neurons in the anterolateral part of entorhinal cortex layer II (alEC LII) are the predominant cortical site for hyperphosphorylation of tau (p-tau) and formation of neurofibrillary tangles (NFTs) in brains of subjects with early-stage Alzheimer’s Disease (AD). A majority of alEC LII-neurons are unique among cortical excitatory neurons b...
All disease-targeting drug trials completed to date have fallen short of meeting the clinical endpoint of significantly slowing cognitive decline in Alzheimer’s disease patients. Even the recently approved drug Aducanumab, has proven effective in removing amyloid-β, but does not reduce cognitive decline. This emphasizes the urgent need for novel th...
Background:
Preclinical models of Alzheimer's disease (AD) can provide valuable insights into the onset and progression of the disease, such as changes in concentrations of amyloid-β (Aβ) and tau in cerebrospinal fluid (CSF). However, such models are currently underutilized due to limited advancement in techniques that allow for longitudinal CSF m...
Background
Preclinical models of Alzheimer’s disease (AD) can provide valuable insights into the onset and progression of the disease, such as changes in concentrations of amyloid-β (Aβ) and tau in cerebrospinal fluid (CSF). However, such models are currently underutilized due to limited advancement in techniques that allow for longitudinal monitor...
Preclinical models of Alzheimer's disease (AD) can provide valuable insights into the onset and progression of the disease, such as changes in concentrations of amyloid-β (Aβ) and tau in cerebrospinal fluid (CSF). However, such models are currently underutilized due to limited advancement in techniques that allow for longitudinal monitoring of CSF...
Alzheimer’s disease (AD) is a debilitating neurodegenerative disease characterized by the accumulation of two proteins in fibrillar form: amyloid-β (Aβ) and tau. Despite decades of intensive research, we cannot yet pinpoint the exact cause of the disease or unequivocally determine the exact mechanism(s) underlying its progression. This confounds ea...