Evidence map›Paper›PMID 38450239›Full record

ReviewFrontiers in nutrition2024

Deficiencies in one-carbon metabolism led to increased neurological disease risk and worse outcome: homocysteine is a marker of disease state.

Sanika M Joshi, Nafisa M Jadavji

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 12 citations in OpenAlex.

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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

2 authors at 2 institutions in 2 countries.

Sanika M JoshiCollege of Osteopathic Medicine, Midwestern University, Glendale, AZ, United States.
Nafisa M JadavjiCollege of Osteopathic Medicine, Midwestern University, Glendale, AZ, United States.
Midwestern University · USUniversity of Phoenix · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated plasma homocysteine levels have been identified as a significant, independent risk factor for the development of cognitive decline including Alzheimer's disease. While several studies have explored the link between homocysteine and disease risk, the associations have not been entirely clear. Elevated levels of homocysteine serve as a disease marker and understanding the underlying cause of these increased levels (e.g., dietary or genetic deficiency in one-carbon metabolism, 1C) will provide valuable insights into neurological disease risk and outcomes. Previous cell culture experiments investigating the mechanisms involved used ultra-high levels of homocysteine that are not observed in human patients. These studies have demonstrated the negative impacts of ultra-high levels of homocysteine can have on for example proliferation of neuroprogenitor cells in the adult hippocampus, as well as triggering neuronal apoptosis through a series of events, including DNA damage, PARP activation, NAD depletion, mitochondrial dysfunction, and oxidative stress. The aim of this mini-review article will summarize the literature on deficiencies in 1C and how they contribute to disease risk and outcomes and that homocysteine is a marker of disease.

Indexed as

cognitive declinefolatefolic acidhomocysteineischemic strokeone-carbon metabolism

Identifiers

PMID38450239
PMCPMC10915003
OpenAlexW4392002384

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.