Evidence map›Paper›PMID 38253804›Full record

ArticleNeuropsychopharmacology reports2024

Marked alteration of phosphoinositide signaling-associated molecules in postmortem prefrontal cortex with bipolar disorder.

Mizuki Hino, Yasuto Kunii, Risa Shishido, Atsuko Nagaoka, Junya Matsumoto, Hiroyasu Akatsu, Yoshio Hashizume, Hideki Hayashi, Akiyoshi Kakita, Hiroaki Tomita and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropsychopharmacology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 5 institutions in 1 country.

Mizuki HinoDepartment of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan.ORCID https://orcid.org/0000-0003-3700-0322
Yasuto KuniiDepartment of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan.
Risa ShishidoDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Atsuko NagaokaDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.ORCID https://orcid.org/0000-0002-1159-4436
Junya MatsumotoDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.ORCID https://orcid.org/0000-0003-4228-3208
Hiroyasu AkatsuDepartment of Community-Based Medical Education/Department of Community-Based Medicine, Nagoya City University Graduate School of Medical Science, Nagoya, Aichi, Japan.
Yoshio HashizumeChoju Medical Institute, Fukushimura Hospital, Toyohashi, Aichi, Japan.
Hideki HayashiDepartment of Pathology, Brain Research Institute, Niigata University, Niigata, Japan.
Akiyoshi KakitaDepartment of Pathology, Brain Research Institute, Niigata University, Niigata, Japan.
Hiroaki TomitaDepartment of Psychiatry, Graduate School of Medicine, Tohoku University, Sendai, Miyagi, Japan.
Hirooki YabeDepartment of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan.
Fukushima Medical University · JPNiigata University · JPTohoku University · JPFukushimura Hospital · JPNagoya City University · JP

Funding

Collaborative Research Project of the Brain Research Institute, Niigata University 22002Japan Agency for Medical Research and Development JP22dm0207074Japan Agency for Medical Research and Development JP22wm0425019Japan Society for the Promotion of Science JP21H00180Japan Society for the Promotion of Science JP21K07524
6 · The paper itself

Abstract

aimThe etiology of bipolar disorder (BD) remains unknown; however, lipid abnormalities in BD have received increasing attention in recent years. In this study, we examined the expression levels of enzyme proteins associated with the metabolic pathway of phosphoinositides (PIs) and their downstream effectors, protein kinase B (Akt1) and glycogen synthase kinase 3β (GSK3β), which have been assumed to be the targets of mood stabilizers such as lithium, in the postmortem brains of patients with BD.

methodsThe protein expression levels of phosphatidylinositol 4-phosphate 5-kinase type-1 gamma (PIP5K1C), phosphatidylinositol 4-kinase alpha (PIK4CA), phosphatase and tensin homolog deleted from chromosome 10 (PTEN), Akt1, and GSK3β were measured using enzyme-linked immunosorbent assays and multiplex fluorescent bead-based immunoassays in the prefrontal cortex (PFC). Specifically, PTEN, Akt1, GSK3β, and PIP5K1C were measured in seven BD patients and 48 controls. Additionally, PIK4CA was analyzed in 10 cases and 34 controls.

resultsPTEN expression levels were markedly decreased in the PFCs of patients with BD, whereas those of Akt and GSK3β were prominently elevated. Moreover, patients medicated with lithium exhibited higher Akt1 expression levels and lower PTEN expression levels in comparison with the untreated group.

conclusionOur results suggest that the expression levels of Akt1/GSK3β and its upstream regulator PTEN are considerably altered.

Indexed as

Bipolar DisorderGlycogen Synthase Kinase 3 betaHumansLithiumPrefrontal CortexSignal TransductionGlycogen Synthase Kinase 3 betaLithiumAktbipolar disorderGSK3βlithiumphosphoinositidespostmortem brainprefrontal cortexPTEN

Identifiers

PMID38253804
PMCPMC10932789
OpenAlexW4391115088

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.