Evidence map›Paper›PMID 40700403›Full record

ReviewACS chemical biology2025

Neutral pH-Selective Inhibition of Cytosolic Cathepsin B: A Novel Drug Targeting Strategy for Traumatic Brain Injury and Alzheimer's Disease.

Vivian Hook, Sonia Podvin, Michael C Yoon, Von V Phan, Jazmin Florio, Brian Spencer, Charles Mosier, Adeline Cheng, Sarah Ahuett, Jehad Almaliti and 3 more

Abstract readReview
In one paragraph

Review in ACS chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

13 authors.

Vivian HookSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.ORCID 0000-0001-6461-7024
Sonia PodvinSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.
Michael C YoonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.ORCID 0000-0002-2900-5257
Von V PhanSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.
Jazmin FlorioDepartment of Physiology and Neuroscience, USC Alzheimer's Therapeutic Research Institute, San Diego, California 92121, United States.
Brian SpencerDepartment of Physiology and Neuroscience, USC Alzheimer's Therapeutic Research Institute, San Diego, California 92121, United States.
Charles MosierSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.
Adeline ChengSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.ORCID 0009-0009-0852-7935
Sarah AhuettSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.
Jehad AlmalitiCenter for Maine Biotechnology and Biomedicine, Scripps Institution of Oceanography, University of California, La Jolla, San Diego, California 92093, United States.
William H GerwickCenter for Maine Biotechnology and Biomedicine, Scripps Institution of Oceanography, University of California, La Jolla, San Diego, California 92093, United States.
Robert A RissmanDepartment of Physiology and Neuroscience, USC Alzheimer's Therapeutic Research Institute, San Diego, California 92121, United States.
Anthony J O'DonoghueSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, La Jolla, San Diego, California 92093, United States.

Funding

USCADRC Diversity Supplement PachicanoP30AG066530 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Hussein N Yassine · 2020 to 2026
$27.8M
Development of Molecular Probe Inhibitors of Pathogenic, Cytosolic Cathespin B in Traumatic Brain Injury and Alzheimers Disease NeurodegenerationR01NS109075 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOOK, VIVIAN Y. H · 2019 to 2023
$3.7M
Impact of TBI and Cognitive Decline on Alzheimer's Disease Brain-Derived Exosome CargoRF1AG079303 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RISBROUGH, VICTORIA B, RISSMAN, ROBERT · 2023 to 2023
$1.9M
Screening of US and Jordanian Natural Product Libraries for the Discovery of Blood Brain Barrier (BBB) Penetrant Cathepsin L Inhibitors for the Treatment of Chronic PainR21AT013004 · NCCIH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ALMALITI, JEHAD S, GERWICK, WILLIAM HENRY · 2024 to 2024
$342k
NCCIH NIH HHS R21 AT013004NIA NIH HHS P30 AG066530NIA NIH HHS RF1 AG079303NINDS NIH HHS R01 NS109075
6 · The paper itself

Abstract

Cathepsin B contributes to the behavioral deficits and neuropathology that occur in traumatic brain injury (TBI) and Alzheimer's disease (AD). TBI and AD patients display elevated levels of cathepsin B that correlate with the severity of injury or cognitive deficits, respectively. In animal models of TBI and AD, cathepsin B gene knockout ameliorates behavioral deficits and improves neuropathology. While cathepsin B is normally located in acidic lysosomes, during TBI and AD, lysosomal leakage results in the translocation of cathepsin B to the neutral pH environment of the cytosol, thereby initiating neurodegeneration. Neutral pH-selective inhibitors are hypothesized to specifically target the pathogenic cytosolic cathepsin B without affecting its normal lysosomal form. Therefore, this review focuses on a novel strategy to utilize pH-dependent substrate cleavage properties of cathepsin B for the design of a neutral pH-selective inhibitor. Investigation of the enzymatic properties of cathepsin B at different pH conditions led to the development of Z-Arg-Lys-AOMK, a neutral pH-selective inhibitor that does not affect the enzyme's activity at normal lysosomal acidic pH. Z-Arg-Lys-AOMK potently inhibits cathepsin B at nM concentrations and effectively inhibits cellular cathepsin B in neuronal cell cultures at similar levels. In mice subjected to controlled cortical impact (CCI) brain injury, a model of TBI, cytosolic cathepsin B activity was significantly elevated in the brain. Treatment of the CCI-TBI mice with Z-Arg-Lys-AOMK reduced cytosolic cathepsin B activity and resulted in less motor dysfunction. These findings show that pH-dependent cleavage properties of cathepsin B can be utilized for the development of selective inhibitors to target the neutral cytosolic form of cathepsin B. The new concept of pH-selective inhibitors of cathepsin B reveals novel opportunities for targeting pathogenic, cytosolic cathepsin B involved in brain disorders.

Indexed as

Alzheimer DiseaseBrain Injuries, TraumaticCathepsin BCytosolAnimalsHumansHydrogen-Ion ConcentrationLysosomesMiceCathepsin B

Identifiers

PMID40700403
PMCPMC12362428

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.