Evidence map›Paper›PMID 37505397›Full record

ReviewJournal of pharmacokinetics and pharmacodynamics2024

Computational neurosciences and quantitative systems pharmacology: a powerful combination for supporting drug development in neurodegenerative diseases.

Hugo Geerts, Silke Bergeler, William W Lytton, Piet H van der Graaf

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of pharmacokinetics and pharmacodynamics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Editor's note on the themed issue: assessing QSP models and amplifying their impact.Journal of pharmacokinetics and pharmacodynamics · 2024
    Article
  6. Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024
    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

4 authors at 2 institutions in 1 country.

Hugo GeertsCertara-US, Princeton, USA. hugo.geerts@certara.com.
Silke BergelerCertara-US, Princeton, USA.
William W LyttonDownstate Health Science University, State University of New York, Brooklyn, USA.
Piet H van der GraafCertara-UK, Canterbury, UK.
Certara (United States) · USState University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Successful clinical development of new therapeutic interventions is notoriously difficult, especially in neurodegenerative diseases, where predictive biomarkers are scarce and functional improvement is often based on patient's perception, captured by structured interviews. As a consequence, mechanistic modeling of the processes relevant to therapeutic interventions in CNS disorders has been lagging behind other disease indications, probably because of the perceived complexity of the brain. However in this report, we develop the argument that a combination of Computational Neurosciences and Quantitative Systems Pharmacology (QSP) modeling of molecular pathways is a powerful simulation tool to enhance the probability of successful drug development for neurodegenerative diseases. Computational Neurosciences aims to predict action potential dynamics and neuronal circuit activation that are ultimately linked to behavioral changes and clinically relevant functional outcomes. These processes can not only be affected by the disease state, but also by common genotype variants on neurotransmitter-related proteins and the psycho-active medications often prescribed in these patient populations. Quantitative Systems Pharmacology (QSP) modeling of molecular pathways allows to simulate key pathological drivers of dementia, such as protein aggregation and neuroinflammatory responses. They often impact neurotransmitter homeostasis and voltage-gated ion-channels or lead to mitochondrial dysfunction, ultimately leading to changes in action potential dynamics and clinical readouts. Combining these two modeling approaches can lead to better actionable understanding of the many non-linear pharmacodynamic processes active in the human diseased brain. Practical applications include a rational selection of the optimal doses in combination therapies, identification of subjects more likely to respond to treatment, a more balanced stratification of treatment arms in terms of comedications, disease status and common genotype variants and re-analysis of small clinical trials to uncover a possible clinical signal. Ultimately this will lead to a higher success rate of bringing new therapeutics to the right patient populations.

Indexed as

Drug DevelopmentNeurodegenerative DiseasesAnimalsBrainComputational BiologyComputer SimulationHumansNetwork PharmacologyNeurosciencesSystems BiologyADAS-CogAlzheimerBiomarkerPredictive modeling

Identifiers

PMID37505397
OpenAlexW4385330209

What OpenQuestion holds

Textmetadata
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.