AI Article Synopsis
- Protein aggregation is a key factor in Alzheimer's disease, but how it starts in living organisms is not well understood.
- Researchers found that injecting diluted brain extracts rich in amyloid-beta from humans or mice with Alzheimer's led to the development of beta-amyloidosis in mice, influenced by the timing and concentration of the extract.
- The study suggests that the induced amyloidosis varies based on the type of brain extract and the host, indicating the presence of different strains of amyloid-beta similar to the variety seen in prion diseases.
Article Abstract
Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1126/science.1131864 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Oxidative/Nitrosative Stress, Apoptosis, and Redox Signaling: Key Players in Neurodegenerative Diseases.
J Biochem Mol Toxicol
January 2025
Department of Medical Biochemistry, Faculty of Medicine, Kahramanmaraş Sütçü İmam University, Kahramanmaraş, Turkey.
Neurodegenerative diseases are significant health concerns that have a profound impact on the quality and duration of life for millions of individuals. These diseases are characterized by pathological changes in various brain regions, specific genetic mutations associated with the disease, deposits of abnormal proteins, and the degeneration of neurological cells. As neurodegenerative disorders vary in their epidemiological characteristics and vulnerability of neurons, treatment of these diseases is usually aimed at slowing disease progression.
View Article and Find Full Text PDFPreliminary Evidence for Perturbation-Based tACS-EEG Biomarkers of Gamma Activity in Alzheimer's Disease.
Int J Geriatr Psychiatry
January 2025
Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Background: Alzheimer's disease (AD) is characterized by impaired inhibitory circuitry and GABAergic dysfunction, which is associated with reduced fast brain oscillations in the gamma band (γ, 30-90 Hz) in several animal models. Investigating such activity in human patients could lead to the identification of novel biomarkers of diagnostic and prognostic value. The current study aimed to test a multimodal "Perturbation-based" transcranial Alternating Current Stimulation-Electroencephalography (tACS)-EEG protocol to detect how responses to tACS in AD patients correlate with patients' clinical phenotype.
View Article and Find Full Text PDFObtaining personalized predictions from a randomized controlled trial on Alzheimer's disease.
Sci Rep
January 2025
TauRx Therapeutics, Aberdeen, Scotland.
The purpose of this article is to infer patient level outcomes from population level randomized control trials (RCTs). In this pursuit, we utilize the recently proposed synthetic nearest neighbors (SNN) estimator. At its core, SNN leverages information across patients to impute missing data associated with each patient of interest.
View Article and Find Full Text PDFDepression and dementia: interrogating the causality of the relationship.
J Neurol Neurosurg Psychiatry
January 2025
Wolfson Institute of Population Health, Queen Mary University of London, London, UK.
Background: Depression is often cited as a major modifiable risk factor for dementia, though the relative contributions of a true causal relationship, reverse causality and confounding factors remain unclear. This study applied a subset of the Bradford Hill criteria for causation to depression and dementia including strength of effect, specificity, temporality, biological gradient and coherence.
Methods: A total of 491 557 participants in UK Biobank aged between 40 and 69 at enrolment and followed up for a mean duration of 12.
Expanding perspectives on the relationship between statin potency and lipophilicity in Alzheimer's disease management.
Pharmacol Res
January 2025
Department of Clinical Pharmacy, Xiangtan Central Hospital (The affiliated hospital of Hunan university), Xiangtan 411100, China. Electronic address:
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!