Evidence map›Paper›PMID 31757935›Full record

ArticleAging2019

Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism.

Xin Lv, Xinyan Wang, Yalan Wang, Dezheng Zhou, Wen Li, John X Wilson, Hong Chang, Guowei Huang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

8 authors at 2 institutions in 2 countries.

Xin LvDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Xinyan WangDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Yalan WangDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Dezheng ZhouDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Wen LiDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
John X WilsonDepartment of Exercise and Nutrition Sciences, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY 14214, USA.
Hong ChangDepartment of Rehabilitation Medicine, Tianjin Medical University, Tianjin 300070, China.
Guowei HuangDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Tianjin Medical University · CNUniversity at Buffalo, State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The occurrence of telomere attrition in brain may cause senescence and death of neurons, leading to cognitive decline. Folic acid (FA) has been reported to improve cognitive performance in mild cognitive impairment; however, its association with telomere remains unclear. The study aimed to investigate if alleviation of telomere attrition by FA supplementation could act as a potential mechanism to delay age-related cognitive decline in senescence-accelerated mouse prone 8 (SAMP8). Aged SAMP8 mice were assigned to four treatment groups: FAdeficient diet (FA-D) group, FA-normal diet (FA-N) group, low FA-supplemented diet (FA-L) group and high FAsupplemented diet (FA-H) group. There was also an age-matched senescence-accelerated mouse resistant 1 (SAMR1) control group (Con-R), and a young SAMP8 control group (Con-Y). The results demonstrated that FA supplementation delayed age-related cognitive decline and neurodegeneration in SAMP8 mice. Importantly, this effect could be attributed to the alleviated telomere attrition, which might be interpreted by the decreased levels of reactive oxygen species. Additionally, improved telomere integrity stimulated mitochondrial function via telomere-p53-mithondria pathway, consequently delayed neuronal degeneration. In conclusion, we demonstrate that FA supplementation delays age-related neurodegeneration and cognitive decline in SAMP8 mice, in which alleviated telomere attrition could serve as one influential factor in the process.

Indexed as

Cognitive DysfunctionDietary SupplementsAgingAnimalsBrainFolic AcidMaleMiceNerve DegenerationTelomere ShorteningFolic Acidcognitive declinefolic acidmitochondrial dysfunctionneurodegenerationtelomere attrition

Identifiers

PMID31757935
PMCPMC6914419
OpenAlexW2991438228

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.