Evidence map›Paper›PMID 33624140›Full record

ArticleMolecular neurobiology2021

Mitochondrial PKA Is Neuroprotective in a Cell Culture Model of Alzheimer's Disease.

Tania Das Banerjee, Kelly Reihl, Maryann Swain, Mariana Torres, Ruben K Dagda

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2021. 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
1.6field-weighted citation impact, top 16% 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. Signaling architecture of the glucagon-like peptide-1 receptor.The Journal of clinical investigation · 2026
    Review
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  12. The Effective Components, Core Targets, and Key Pathways of Ginseng against Alzheimer's Disease.Evidence-based complementary and alternative medicine : eCAM · 2023
    Article
  13. Article
  14. Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021
    Review
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 1 institution in 1 country.

Tania Das BanerjeeDepartment of Pharmacology, Reno School of Medicine, University of Nevada, Reno, NV, 89557, USA.
Kelly ReihlDepartment of Pharmacology, Reno School of Medicine, University of Nevada, Reno, NV, 89557, USA.ORCID https://orcid.org/0000-0001-8980-8062
Maryann SwainDepartment of Pharmacology, Reno School of Medicine, University of Nevada, Reno, NV, 89557, USA.ORCID https://orcid.org/0000-0002-3094-098X
Mariana TorresDepartment of Pharmacology, Reno School of Medicine, University of Nevada, Reno, NV, 89557, USA.
Ruben K DagdaDepartment of Pharmacology, Reno School of Medicine, University of Nevada, Reno, NV, 89557, USA. rdagda@med.unr.edu.ORCID http://orcid.org/0000-0002-9946-9591
University of Nevada, Reno · US

Funding

Outreach/Diversity/Pipeline ProjectP20GM103440 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Julia Petereit · 2012 to 2026
$58.0M
Cell Biology of Signaling across MembranesP20GM103554 · NIGMS · UNIVERSITY OF NEVADA RENO · PI VON BARTHELD, CHRISTOPHER S · 2012 to 2016
$8.0M
Regulation of Dendrite Homeostasis by PINK1 and PKA in Models of Parkinson's DiseaseR01NS105783 · NINDS · UNIVERSITY OF NEVADA RENO · PI DAGDA, RUBEN K · 2018 to 2022
$1.9M
NIGMS NIH HHS GM103554NIGMS NIH HHS P20 GM103440NIGMS NIH HHS P20 GM103554NINDS NIH HHS 1R01NS105783NINDS NIH HHS R01 NS105783
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and cognitive decline. In hippocampal neurons, the pathological features of AD include the accumulation of extracellular amyloid-beta peptide (Aβ) accompanied by oxidative stress, mitochondrial dysfunction, and neuron loss. A decrease in neuroprotective Protein Kinase A (PKA) signaling contributes to mitochondrial fragmentation and neurodegeneration in AD. By associating with the protein scaffold Dual-Specificity Anchoring Protein 1 (D-AKAP1), PKA is targeted to mitochondria to promote mitochondrial fusion by phosphorylating the fission modulator dynamin-related protein 1 (Drp1). We hypothesized that (1) a decrease in the endogenous level of endogenous D-AKAP1 contributes to decreased PKA signaling in mitochondria and that (2) restoring PKA signaling in mitochondria can reverse neurodegeneration and mitochondrial fragmentation in neurons in AD models. Through immunohistochemistry, we showed that endogenous D-AKAP1, but not other mitochondrial proteins, is significantly reduced in primary neurons treated with Aβ

Indexed as

A Kinase Anchor ProteinsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCells, CulturedCyclic AMP-Dependent Protein KinasesFemaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaNeuroprotectionPeptide FragmentsPregnancyRatsAkap1 protein, mouseA Kinase Anchor ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Cyclic AMP-Dependent Protein KinasesPeptide FragmentsAlzheimer’s diseaseD-AKAP1MitochondriaNeurodegenerationOxidative stressPKA

Identifiers

PMID33624140
PMCPMC8260456
OpenAlexW3129243063

What OpenQuestion holds

Textmetadata
LicenceTDM
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.