ArticleJournal of neuropathology and experimental neurology2015
Prion Disease Induces Alzheimer Disease-Like Neuropathologic Changes.
Article in Journal of neuropathology and experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Tau oligomers impair memory and synaptic plasticity through the cellular prion protein.Acta neuropathologica communications · 2025Article
- Decellularization of various tissues and organs through chemical methods.Tissue & cell · 2024Review
- Cerebrospinal fluid p-tau181, 217, and 231 in definite Creutzfeldt-Jakob disease with and without concomitant pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Identification of high-performing antibodies for the reliable detection of Tau proteoforms by Western blotting and immunohistochemistry.Acta neuropathologica · 2024Article
- Histoblot: A sensitive method to quantify the expression of proteins in normal and pathological conditions.Histology and histopathology · 2023Review
- Selective vulnerability to atrophy in sporadic Creutzfeldt-Jakob disease.Annals of clinical and translational neurology · 2021Article
- Sporadic Creutzfeldt-Jakob Disease and Other Proteinopathies in Comorbidity.Frontiers in neurology · 2020Article
- Production of seedable Amyloid-β peptides in model of prion diseases upon PrPNature communications · 2019Article
- "Dual Disease" TgAD/GSS mice exhibit enhanced Alzheimer's disease pathology and reveal PrPScientific reports · 2019Article
- Early-onset Alzheimer's disease patient with prionNeuropsychiatric disease and treatment · 2019Article
- Co-occurrence of chronic traumatic encephalopathy and prion disease.Acta neuropathologica communications · 2018Article
- Prion Diseases.Neurologic clinics · 2018Review
- An autopsy report of three kindred in a Gerstmann-Sträussler-Scheinker disease P105L family with a special reference to prion protein, tau, and beta-amyloid.Brain and behavior · 2018Article
- Cerebrospinal fluid and blood biomarkers for neurodegenerative dementias: An update of the Consensus of the Task Force on Biological Markers in Psychiatry of the World Federation of Societies of Biological Psychiatry.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2018Review
- Genetic PrP Prion Diseases.Cold Spring Harbor perspectives in biology · 2018Review
- Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study.Acta neuropathologica communications · 2018Article
- Different Molecular Mechanisms Mediate Direct or Glia-Dependent Prion Protein Fragment 90-231 Neurotoxic Effects in Cerebellar Granule Neurons.Neurotoxicity research · 2017Article
- Tau pathology in Creutzfeldt-Jakob disease revisited.Brain pathology (Zurich, Switzerland) · 2017Article
- Genetic prion disease: Experience of a rapidly progressive dementia center in the United States and a review of the literature.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017Review
- Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We examined the brains of 266 patients with prion disease (PrionD) and found that 46 patients (17%) had Alzheimer disease (AD)-like changes. To explore potential mechanistic links between PrionD and AD, we exposed human brain aggregates (BrnAggs) to a brain homogenate from a patient with sporadic Creutzfeldt-Jakob disease and found that neurons in human BrnAggs produced many β-amyloid (Aβ; Aβ42) inclusions, whereas uninfected control-exposed human BrnAggs did not. Western blot analysis of 20 pooled Creutzfeldt-Jakob disease-infected BrnAggs verified Aβ42 levels higher than those in controls. We next examined the CA1 region of the hippocampus from 14 patients with PrionD and found that 5 patients had low levels of scrapie-associated prion protein (PrP), many Aβ42 intraneuronal inclusions, low apolipoprotein E-4 (APOE-4), and no significant nerve cell loss. Seven patients had high levels of PrP, low Aβ42, high APOE-4, and 40% nerve cell loss, suggesting that APOE-4 and PrP together cause neuron loss in PrionD. There were also increased levels of hyperphosphorylated tau protein (Hτ) and Hτ-positive neuropil threads and neuron bodies in both PrionD and AD groups. The brains of 6 age-matched control patients without dementia did not contain Aβ42 deposits; however, there were rare Hτ-positive threads in 5 controls, and 2 controls had few Hτ-positive nerve cell bodies. We conclude that PrionD may trigger biochemical changes similar to those triggered by AD and suggest that PrionD is a disease involving PrP, Aβ42, APOE-4, and abnormal tau.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.