ArticleInternational journal of molecular sciences2024
Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Ischemic Stroke and Traumatic Brain Injury: Epidemiology, Molecular Pathways, and Emerging Therapies.MedComm · 2026Review
- Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy.JAMA network open · 2026Article
- Oral Supplementation With a Bovine Thymus Extract Reduces Neuronal Excitability in Aging Mice.FASEB bioAdvances · 2026Article
- MSC-Exosomes alleviate cognitive impairment after mild traumatic brain injury by inhibiting ferroptosis via PI3K/AKT/mTOR-mediated upregulation of GPX4.Functional & integrative genomics · 2025Article
- Genetic Differences Modify Anesthetic Preconditioning of Traumatic Brain Injury in Drosophila.Journal of neurotrauma · 2025Article
- Review
- Nanoparticles as an Encouraging Therapeutic Approach to Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Decreased IL-33 in the brain following repetitive mild traumatic brain injury contributes to cognitive impairment by inhibiting microglial phagocytosis.Military Medical Research · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This editorial investigates chronic traumatic encephalopathy (CTE) as a course of Alzheimer's disease (AD). CTE is a debilitating neurodegenerative disease that is the result of repeated mild traumatic brain injury (TBI). Many epidemiological studies show that experiencing a TBI in early or middle life is associated with an increased risk of dementia later in life. Chronic traumatic encephalopathy (CTE) and Alzheimer's disease (AD) present a series of similar neuropathological features that were investigated in this work like recombinant tau into filaments or the accumulation and aggregation of Aβ protein. However, these two conditions differ from each other in brain-blood barrier damage. The purpose of this review was to evaluate information about CTE and AD from various articles, focusing especially on new therapeutic possibilities for the improvement in cognitive skills.
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Registered trials
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.