Sarah K. Fritschi

ORCID: 0000-0003-4665-7203
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Prion Diseases and Protein Misfolding
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Parkinson's Disease Mechanisms and Treatments
  • Neurological diseases and metabolism
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Sleep and Wakefulness Research
  • Alcoholism and Thiamine Deficiency
  • Neuroscience and Neuropharmacology Research
  • Functional Brain Connectivity Studies
  • Dementia and Cognitive Impairment Research
  • Aluminum toxicity and tolerance in plants and animals
  • Endoplasmic Reticulum Stress and Disease
  • Point processes and geometric inequalities
  • Tryptophan and brain disorders
  • Cholinesterase and Neurodegenerative Diseases

University of Tübingen
2011-2020

Hertie Institute for Clinical Brain Research
2011-2020

German Center for Neurodegenerative Diseases
2011-2019

Hope Center for Neurological Disorders
2019

TH Bingen University of Applied Sciences
2011

Sleep may protect the brain from AD Two main proteins accumulate in Alzheimer's disease (AD), β-amyloid (Aβ) and tau. Aβ appears to instigate AD, but tau drive damage cognitive decline. deprivation is known increase acutely chronically. Now, Holth et al. show that chronic sleep strongly increases over hours also drives pathology spreading brains of mice humans (see Perspective by Noble Spires-Jones). Thus, have a direct protective effect on key protein pathology. Science , this issue p. 880 ; see 813

10.1126/science.aav2546 article EN Science 2019-01-25

Cerebral β-amyloidosis and associated pathologies can be exogenously induced by the intracerebral injection of small amounts pathogenic Aβ-containing brain extract into young β-amyloid precursor protein (APP) transgenic mice. The probable β-amyloid-inducing factor in has been identified as a species aggregated Aβ that is generated its most effective conformation or composition vivo. Here we report more proteinase K (PK) resistant than synthetic fibrillar Aβ, this PK-resistant fraction...

10.1523/jneurosci.3088-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-10-12

Deposition of aggregated amyloid-β (Aβ) peptide in brain is an early event and hallmark pathology Alzheimer9s disease cerebral Aβ angiopathy. Experimental evidence supports the concept that multimers can act as seeds structurally corrupt other peptides by a self-propagating mechanism. Here we compare induction β-amyloidosis intraperitoneal applications Aβ-containing extracts three Aβ-precursor protein (APP) transgenic mouse lines differ levels transgene expression periphery (APP23 mice,...

10.1523/jneurosci.1608-14.2014 article EN Journal of Neuroscience 2014-07-30

The soluble fraction of brain samples from patients with Alzheimer's disease contains highly biologically active amyloid-β seeds. In this study, we sought to assess the potency seeds derived and cerebrospinal fluid. Soluble extracts were serially diluted then injected into hippocampus young, APP transgenic mice. Eight months later, seeded deposition was evident even when received subattomole amounts brain-derived amyloid-β. contrast, fluid disease, which contained more than 10-fold higher...

10.1093/brain/awu255 article EN Brain 2014-09-10

Abstract An important early event in the pathogenesis of A lzheimer's disease ( AD ) is aberrant polymerization and extracellular accumulation amyloid‐β peptide β). In young transgenic mice expressing human β‐precursor protein APP ), deposits β can be induced by inoculation minute amounts brain extract containing aggregates (“ seeds”), indicative a prion‐like seeding phenomenon. Moreover, focal intracerebral injection seeds induce not only immediate vicinity site, but, with time, also distal...

10.1111/bpa.12252 article EN Brain Pathology 2015-02-12

In vivo imaging of pathological protein aggregates provides essential knowledge the kinetics and implications these lesions in progression proteopathies, such as Alzheimer disease. Luminescent conjugated oligothiophenes are amyloid-specific ligands that bind spectrally distinguish different types amyloid aggregates. Herein, we report heptamer formyl thiophene acetic acid (hFTAA) passes blood-brain barrier after systemic administration specifically binds to extracellular β-amyloid deposits...

10.1016/j.ajpath.2012.08.031 article EN cc-by-nc-nd American Journal Of Pathology 2012-10-04

Clinical trials targeting β-amyloid peptides (Aβ) for Alzheimer disease (AD) failed arguable reasons that include selecting the wrong stages of AD pathophysiology or Aβ being target. Targeting to prevent cerebral amyloid angiopathy (CAA) has not been rigorously followed, although causal role CAA and related hemorrhages is undisputed. occurs with normal aging various degrees in AD, where its impact treatment confounded by presence parenchymal deposition.APPDutch mice develop absence amyloid,...

10.1002/ana.25562 article EN cc-by-nc Annals of Neurology 2019-07-30

Background: An accurate prognosis of decline is essential to reduce the dementia related burden by timely access formal advice and care.The purpose this study determine added diagnostic value cerebrospinal fluid (CSF) a clinical judgment for prediction cognitive or functional decline.Methods: In prospective cohort memory clinic patients were evaluated at baseline according current standard evaluations (physical, neuropsychological examination, history, MRI) received CSF test.A pathway...

10.1016/j.jalz.2014.05.1580 article EN Alzheimer s & Dementia 2014-07-01

The commonality of many neurodegenerative disorders is the predictable temporal occurrence and progression specific aggregated proteins in brain. hallmark proteopathy Alzheimer’s disease which amyloid-β peptide (Aβ) deposited brain parenchyma as amyloid plaques. Multiple evidence suggests that β-amyloidosis induced by Aβ can spread within among regions act corruptive templates (seeds) induce a chain-reaction misfolding aggregation. insight prion paradigm may also apply to cerebral other...

10.1186/1750-1326-8-s1-o21 article EN cc-by Molecular Neurodegeneration 2013-01-01

Cerebral amyloid angiopathy (CAA) is frequently exhibited in patients suffering from Alzheimer's disease, Down syndrome, or hereditary cerebral hemorrhage with amyloidosis - Dutch type (HCHWA-D). The latter characterized by the E693Q (Dutch) mutation precursor protein (APP). APP initially cleaved BACE1 (β-site protein-cleaving enzyme 1), which leads to generation of β-amyloid peptide (Aβ). In HCHWA-D Aβ accumulates blood vessels and leptomeninges. We have previously shown that mice...

10.1016/j.jalz.2017.06.707 article EN Alzheimer s & Dementia 2017-07-01

Junge Menschen in Dirndl und Lederhose auf Volksfesten wie dem Oktoberfest München oder Wasen Stuttgart – die­ser Anblick ist heute keine Seltenheit mehr. Doch was sind die Hinter­gründe dieses Trends? Warum kleiden sich gerade Nicht-Bayern seit Beginn des neuen Jahrtausends bayerischer „Tracht“? Und könnte diese Entwicklung mit den aktuellen gesell­schaftlichen Lebensumständen Pluralität, Globalisierung Individuali­sierung Verbindung stehen? Diesen Fragen nähert Forschungsarbeit an, indem...

10.13141/zfm.2017-8.1008 article DE Medienwelten – Zeitschrift für Medienpädagogik 2018-01-29

Failed clinical trials for Alzheimer's disease (AD) suggest that Aβ aggregation must be targeted at very early stages to effective. Furthermore, the deposition of amyloid per se, as assessed microscopically or via PET imaging, is likely a relatively late manifestation pathogenic process. It not known when initial, pre-amyloid seeds begin form, propagate, and spread through brain, nor has structure initial been defined. We tested variety well-described clinically-tested antibodies their in...

10.1016/j.jalz.2019.09.054 article EN Alzheimer s & Dementia 2019-07-01
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