Abstract
Early diagnosis of Alzheimer`s disease (AD) is currently difficult and involves a complex approach including clinical assessment, neuroimaging, and measurement of amyloid-β (Aβ) and tau levels in cerebrospinal fluid (CSF). A better mechanistic understanding is needed to develop more accurate and even presymptomatic diagnostic tools. It has been shown that Aβ derived from amyloid-containing brain tissue has prion-like properties: it induces misfolding and aggregation of Aβ when injected into human amyloid precursor protein (APP) transgenic mice. In contrast, Aβ in the CSF has been less studied, and it is not clear whether it also exhibits prion-like characteristics, which might provide a sensitive diagnostic tool. Therefore, we collected CSF from APP transgenic mice carrying the Swedish mutation (APP23 mice), and injected it intracerebrally into young mice from the same transgenic line. We found that CSF derived Aβ did not induce increased β-amyloidosis, even after long incubation periods and additional concentration. This suggests that Aβ present in the CSF does not have the same prion-like properties as the Aβ species in the brain.
Keywords: Alzheimer's disease, amyloid-beta, Aβ, prion, cerebrospinal fluid, diagnostics, transgenic mouse models.
Current Alzheimer Research
Title:Amyloid-β in the Cerebrospinal Fluid of APP Transgenic Mice Does not Show Prion-like Properties
Volume: 12 Issue: 9
Author(s): Zhiva Skachokova, Frederik Sprenger, Karin Breu, Dorothee Abramowski, Florence Clavaguera, Jurgen Hench, Matthias Staufenbiel, Markus Tolnay and David T. Winkler
Affiliation:
Keywords: Alzheimer's disease, amyloid-beta, Aβ, prion, cerebrospinal fluid, diagnostics, transgenic mouse models.
Abstract: Early diagnosis of Alzheimer`s disease (AD) is currently difficult and involves a complex approach including clinical assessment, neuroimaging, and measurement of amyloid-β (Aβ) and tau levels in cerebrospinal fluid (CSF). A better mechanistic understanding is needed to develop more accurate and even presymptomatic diagnostic tools. It has been shown that Aβ derived from amyloid-containing brain tissue has prion-like properties: it induces misfolding and aggregation of Aβ when injected into human amyloid precursor protein (APP) transgenic mice. In contrast, Aβ in the CSF has been less studied, and it is not clear whether it also exhibits prion-like characteristics, which might provide a sensitive diagnostic tool. Therefore, we collected CSF from APP transgenic mice carrying the Swedish mutation (APP23 mice), and injected it intracerebrally into young mice from the same transgenic line. We found that CSF derived Aβ did not induce increased β-amyloidosis, even after long incubation periods and additional concentration. This suggests that Aβ present in the CSF does not have the same prion-like properties as the Aβ species in the brain.
Export Options
About this article
Cite this article as:
Skachokova Zhiva, Sprenger Frederik, Breu Karin, Abramowski Dorothee, Clavaguera Florence, Hench Jurgen, Staufenbiel Matthias, Tolnay Markus and Winkler T. David, Amyloid-β in the Cerebrospinal Fluid of APP Transgenic Mice Does not Show Prion-like Properties, Current Alzheimer Research 2015; 12 (9) . https://dx.doi.org/10.2174/1567205012666150710115022
DOI https://dx.doi.org/10.2174/1567205012666150710115022 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Neuroprotective Effects of Tetracyclines: Molecular Targets, Animal Models and Human Disease
CNS & Neurological Disorders - Drug Targets The Multifunctional Mesencephalic Locomotor Region
Current Pharmaceutical Design Anti-inflammatory and Immune Therapy for Alzheimers Disease: Current Status and Future Directions
Current Neuropharmacology Regional Grey Matter Loss and Brain Disconnection Across Alzheimer Disease Evolution
Current Medicinal Chemistry Neuron-to-microglia Crosstalk in Psychiatric Disorders
Current Neuropharmacology Asymptomatic Carriers of Presenilin-1 E318G Variant Show no Cerebrospinal Fluid Biochemical Signs Suggestive of Alzheimer’s disease in a Family with Late-onset Dementia
Current Alzheimer Research Early Intervention in Psychosis: Rationale, Results and Implications for Treatment of Adolescents at Risk
Adolescent Psychiatry Editorial (Thematic Issue: Ceramics, Nanotubes, Advanced Materials: Theoretical and Experimental Structure-Property Relationships: Part V)
Current Physical Chemistry Cardiovascular Drugs and Bone
Current Drug Safety Recent Approaches to Novel Anti-Alzheimer Therapy
Current Pharmaceutical Design Assessment of Acute Coronary Syndromes: Focus on Novel Biomarkers
Current Medicinal Chemistry Antioxidant Therapy for Prevention of Inflammation, Ischemic Reperfusion Injuries and Allograft Rejection
Cardiovascular & Hematological Agents in Medicinal Chemistry Editorial [Hot Topic: Cognition Therapeutics (Guest Editor: Miao-Kun Sun)]
Current Drug Targets - CNS & Neurological Disorders Recent Developments in Natural and Synthetic Drug Research for Alzheimers Disease
Letters in Drug Design & Discovery Mitochondrial Serine Protease HtrA2/Omi as a Potential Therapeutic Target
Current Drug Targets Molecular Docking Study of a Series of Substituted Xanthone Derivatives as Novel COX-2 Inhibitors Targeting Prostaglandin Endoperoxide Synthase -2
Current Enzyme Inhibition Importance of ABC Transporters in Drug Development
Current Pharmaceutical Design Dynamic Crosstalk between GlcNAcylation and Phosphorylation: Roles in Signaling, Transcription and Human Disease
Current Signal Transduction Therapy Dyslipidemia, Vascular Atheroma and Statins
Current Vascular Pharmacology Acetylcholinesterase Inhibitors as Disease-Modifying Therapies for Alzheimers Disease
Current Medicinal Chemistry