Evidence map›Paper›PMID 38036591›Full record

ArticleScientific reports2023

Low-dose brain radiation: lowering hyperphosphorylated-tau without increasing DNA damage or oncogenic activation.

Diego Iacono, Erin K Murphy, Cheryl D Stimpson, Daniel P Perl, Regina M Day

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Diego IaconoDoD/USU Brain Tissue Repository and Neuropathology Program, Uniformed Services University (USU), Bethesda, MD, USA. diego.iacono.ctr@usuhs.edu.
Erin K MurphyDoD/USU Brain Tissue Repository and Neuropathology Program, Uniformed Services University (USU), Bethesda, MD, USA.
Cheryl D StimpsonDoD/USU Brain Tissue Repository and Neuropathology Program, Uniformed Services University (USU), Bethesda, MD, USA.
Daniel P PerlDoD/USU Brain Tissue Repository and Neuropathology Program, Uniformed Services University (USU), Bethesda, MD, USA.
Regina M DayDepartment of Pharmacology and Molecular Therapeutics, F. Edward Hébert School of Medicine, Uniformed Services University (USU), Bethesda, MD, USA.
Henry M. Jackson Foundation · USUniformed Services University of the Health Sciences · US

Funding

U.S. Department of Defense D 14 I 14 J7 729U.S. Department of Defense PAT-74-10982
6 · The paper itself

Abstract

Brain radiation has been medically used to alter the metabolism of cancerous cells and induce their elimination. Rarely, though, brain radiation has been used to interfere with the pathomechanisms of non-cancerous brain disorders, especially neurodegenerative disorders. Data from low-dose radiation (LDR) on swine brains demonstrated reduced levels of phosphorylated-tau (CP13) and amyloid precursor protein (APP) in radiated (RAD) versus sham (SH) animals. Phosphorylated-tau and APP are involved in Alzheimer's disease (AD) pathogenesis. We determined if the expression levels of hyperphosphorylated-tau, 3R-tau, 4R-tau, synaptic, intraneuronal damage, and DNA damage/oncogenic activation markers were altered in RAD versus SH swine brains. Quantitative analyses demonstrated reduced levels of AT8 and 3R-tau in hippocampus (H) and striatum (Str), increased levels of synaptophysin and PSD-95 in frontal cortex (FCtx), and reduced levels of NF-L in cerebellum (CRB) of RAD versus SH swine. DNA damage and oncogene activation markers levels did not differ between RAD and SH animals, except for histone-H3 (increased in FCtx and CRB, decreased in Str), and p53 (reduced in FCtx, Str, H and CRB). These findings confirm the region-based effects of sLDR on proteins normally expressed in larger mammalian brains and support the potential applicability of LDR to beneficially interfere against neurodegenerative mechanisms.

Indexed as

Alzheimer Diseasetau ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDNA DamageMammalsPhosphorylationSwineAmyloid beta-PeptidesAmyloid beta-Protein Precursortau Proteins

Identifiers

PMID38036591
PMCPMC10689500
OpenAlexW4389181131

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.