Evidence map›Paper›PMID 23835051›Full record

ArticleBMC neurology2013

Cognitive dysfunction associated with anti-glutamic acid decarboxylase autoimmunity: a case-control study.

Masahito Takagi, Yasushi Ishigaki, Kenji Uno, Shojiro Sawada, Junta Imai, Keizo Kaneko, Yutaka Hasegawa, Tetsuya Yamada, Ai Tokita, Kazumi Iseki and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Function of the GABAergic System in Diabetic Encephalopathy.Cellular and molecular neurobiology · 2023
    Review
  4. Article
  5. Article
  6. Clinical spectrum of high-titre GAD65 antibodies.Journal of neurology, neurosurgery, and psychiatry · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. GAD antibody-associated limbic encephalitis in a young woman with APECED.Endocrinology, diabetes & metabolism case reports · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. 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

14 authors at 2 institutions in 1 country.

Masahito TakagiDepartment of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan. mastakagi@med.tohoku.ac.jp
Yasushi Ishigaki
Kenji Uno
Shojiro Sawada
Junta Imai
Keizo Kaneko
Yutaka Hasegawa
Tetsuya Yamada
Ai Tokita
Kazumi Iseki
Shigenori Kanno
Yoshiyuki Nishio
Hideki Katagiri
Etsuro Mori
Tohoku University Hospital · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the synthesis of γ-aminobutyric acid (GABA). Anti-GAD antibodies (GADA) are associated with the progression of stiff person syndrome and other neurological diseases, as well as the immune-mediated (type 1) diabetes. GABA is one of the most widely distributed neurotransmitters, but the non-motor symptoms of GADA-positive patients are not well understood. Diabetes is increasingly recognized as a risk factor for dementia; however, the relationship between diabetes and dementia is controversial.The objective of this study was to assess cognitive function in patients with GADA-positive diabetes using subjects with GADA-negative type 2 diabetes as controls.

methodsTwenty-one patients with GADA-positive diabetes (mean age 52.5 ± 12.3 years, mean duration 7.7 ± 6.6 years) and 19 control subjects with GADA-negative type 2 diabetes (mean age 53.4 ± 8.9 years, mean duration 12.5 ± 6.7) were included in the study. The subjects underwent extensive neuropsychological testing and brain MRI.

resultsThe neuropsychological test scores were lower in the GADA-positive group than the control group (GADA-negative). Twelve subjects (57%) in the GADA group and 4 subjects (21%) in the control group had low performances (p = 0.027). No statistically significant differences were found between the GADA and control groups regarding demographics, diabetic severity cardiovascular risks, cerebral T2 hyperintensities, white matter volume and gray matter volume.

conclusionsOur study showed that GADA-positive diabetic patients have an increased risk of cognitive decline compared to patients with type 2 diabetes of comparable diabetic severity. It also showed that GADA may be associated with isolated cognitive decline in the absence of other neurological complications.

Indexed as

AdultAgedAge FactorsAnalysis of VarianceAntibodiesAutoimmunityBrainCase-Control StudiesCognition DisordersDiabetes ComplicationsDiabetes MellitusFemaleGlutamate DecarboxylaseHumansLeukoencephalopathiesMagnetic Resonance ImagingAntibodiesGlutamate Decarboxylase

Identifiers

PMID23835051
PMCPMC3711917
OpenAlexW2053734674

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.