Evidence map›Paper›PMID 25176060›Full record

ArticleBiomaterials2014

Effects of caspase-1 knockout on chronic neural recording quality and longevity: insight into cellular and molecular mechanisms of the reactive tissue response.

Takashi D Y Kozai, Xia Li, Lance M Bodily, Ellen M Caparosa, Georgios A Zenonos, Diane L Carlisle, Robert M Friedlander, X Tracy Cui

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
5.0field-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

101 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
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  5. Chronic alteration of CabioRxiv : the preprint server for biology · 2025
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41 more citing papers are in PubMed but not listed here.

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 1 country.

Takashi D Y KozaiBioengineering, University of Pittsburgh, USA; Center for Neural Basis of Cognition, USA; McGowan Institute for Regenerative Medicine, University of Pittsburgh, USA. Electronic address: tdk18@pitt.edu.
Xia LiBioengineering, University of Pittsburgh, USA.
Lance M BodilyNeuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, USA.
Ellen M CaparosaNeuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, USA.
Georgios A ZenonosNeuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, USA.
Diane L CarlisleNeuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, USA.
Robert M FriedlanderNeuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, USA.
X Tracy CuiBioengineering, University of Pittsburgh, USA; Center for Neural Basis of Cognition, USA; McGowan Institute for Regenerative Medicine, University of Pittsburgh, USA. Electronic address: xic11@pitt.edu.
University of Pittsburgh · USMcGowan Institute for Regenerative Medicine · US

Funding

MODULATION OF CASPASE PATHWAYS IN HUNTINGTON'S DISEASER01NS039324 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FRIEDLANDER, ROBERT M. · 2000 to 2014
$5.5M
Improving chronic neural recording performance through biomaterial strategiesR01NS062019 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CUI, XINYAN TRACY · 2008 to 2018
$4.4M
Functional Role of Micro RNAs in Huntington's Disease PathogenesisR01NS077748 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FRIEDLANDER, ROBERT M. · 2012 to 2015
$1.6M
NINDS NIH HHS 5R01NS062019-03NINDS NIH HHS NS077748NINDS NIH HHS R01 NS039324NINDS NIH HHS R01 NS062019NINDS NIH HHS R01 NS077748
6 · The paper itself

Abstract

Chronic implantation of microelectrodes into the cortex has been shown to lead to inflammatory gliosis and neuronal loss in the microenvironment immediately surrounding the probe, a hypothesized cause of neural recording failure. Caspase-1 (aka Interleukin 1β converting enzyme) is known to play a key role in both inflammation and programmed cell death, particularly in stroke and neurodegenerative diseases. Caspase-1 knockout (KO) mice are resistant to apoptosis and these mice have preserved neurologic function by reducing ischemia-induced brain injury in stroke models. Local ischemic injury can occur following neural probe insertion and thus in this study we investigated the hypothesis that caspase-1 KO mice would have less ischemic injury surrounding the neural probe. In this study, caspase-1 KO mice were implanted with chronic single shank 3 mm Michigan probes into V1m cortex. Electrophysiology recording showed significantly improved single-unit recording performance (yield and signal to noise ratio) of caspase-1 KO mice compared to wild type C57B6 (WT) mice over the course of up to 6 months for the majority of the depth. The higher yield is supported by the improved neuronal survival in the caspase-1 KO mice. Impedance fluctuates over time but appears to be steadier in the caspase-1 KO especially at longer time points, suggesting milder glia scarring. These findings show that caspase-1 is a promising target for pharmacologic interventions.

Indexed as

AnimalsApoptosisBrainCaspase 1Foreign-Body ReactionMice, Inbred C57BLMice, KnockoutNeural ProsthesesNeuronsCaspase 1Blood-brain barrierForeign Body ResponseImpedanceMechanical tissue strainOligodendrocytesPericyte

Identifiers

PMID25176060
PMCPMC4174599
OpenAlexW2005893249

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.