Evidence map›Paper›PMID 42468900›Full record

ReviewBiological psychiatry2026

Impaired Activity-Regulated Proteostasis: A Shared Mechanism in Neurodevelopmental Disorders.

Kiran Pandey

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Kiran PandeyDepartment of Pharmacology, Weill Cornell Medicine, Cornell University, New York, New York. Electronic address: kip4006@med.cornell.edu.

Funding

Synthetic Biology in Neurons: Chemogenetic Control of Selective Calcium Signaling in NeuronsR21NS142816 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Kiran Pandey · 2026 to 2026
$466k
A novel RNA-based neuromodulation tool to treat chronic pain and reduce opioid dependenceR21DA066282 · NIDA · WEILL MEDICAL COLL OF CORNELL UNIV · PI Kiran Pandey · 2026 to 2026
$466k
NIDA NIH HHS R21 DA066282NINDS NIH HHS R21 NS142816
6 · The paper itself

Abstract

Proteostasis is the process by which cells control how much of each protein is made, how long it persists, and when it is removed. In neurons, proteostasis is not merely a housekeeping function; it is actively regulated by neuronal activity. When neurons fire, protein synthesis and degradation are simultaneously and transiently regulated to support synaptic plasticity. In neurodevelopmental disorders (NDDs), neurons lose this capacity to dynamically regulate their proteome in response to stimulation, disrupting synaptic plasticity and leading to cognitive impairments. This review establishes that despite diverse genetic origins, failure of activity-regulated proteostasis is a shared vulnerability across NDDs. This framework also explains why increasing or blocking protein synthesis or degradation alone under basal conditions is insufficient to restore normal function. Restoring the coupling between neuronal activity and proteostatic response rescues both molecular and cognitive impairments in NDDs, which offers a new perspective for investigating disease biology and developing novel therapeutic strategies.

Indexed as

Activity-regulated proteostasisNeurodevelopmental disordersNeuronal activityProteostasisProteostasis networkSynaptic plasticity

Identifiers

PMID42468900
PMCPMC13599997

What Socratic 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 Socratic graph.