Evidence map›Paper›PMID 41483162›Full record

ArticlePsychopharmacology2026

3-Methyladenine administration alleviates cognitive and memory dysfunction in attention-deficit/hyperactivity disorder by modulating autophagy.

Ge-Ge Lv, Yu-Dong Shan, Jing-Jing Shao, Cao-Yuan Ma, Zhi-Fang Yu, Ji-Zhen Liu, Li-Min Zhang, Wei Zhang

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

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Ge-Ge Lv *The First Affiliated Hospital of Zhengzhou University, Henan, China.
Yu-Dong Shan *Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Jing-Jing ShaoThe First Affiliated Hospital of Zhengzhou University, Henan, China.
Cao-Yuan MaThe First Affiliated Hospital of Zhengzhou University, Henan, China.
Zhi-Fang YuHebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Ji-Zhen LiuThe First Affiliated Hospital of Zhengzhou University, Henan, China.
Li-Min ZhangHebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China. azai2010@126.com.
Wei ZhangThe First Affiliated Hospital of Zhengzhou University, Henan, China. zhangw1970529@zzu.edu.cn.

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 82171455
6 · The paper itself

Abstract

backgroundAttention-deficit/hyperactivity disorder (ADHD), a highly prevalent neurodevelopmental disorder among children, is directly associated with impairments in cognition and memory. In the nervous system, autophagy is essential for the development of neurons, the formation and remodeling of synapses, and the transmission of neurotransmitters. The 3-methyladenine (3-MA), an autophagy inhibitor, mitigates cognitive and memory impairment in neurological disorders. This study aimed to investigate the potential role of 3-MA in ADHD.

methodsAn ADHD model was established in offspring mice by intraperitoneal injection of S-ketamine during mid-to-late gestation. Postnatal day 14 offspring received intraperitoneal 3-MA (15 mg/kg/day) or vehicle for 7 consecutive days. To assess behavioral, electrophysiological, and pathological changes in mice, several tests were employed, including the open field test (OFT), novel object recognition (NOR) test, fear conditioning (FC), local field potential recording, western blot, transmission electron microscopy and immunofluorescence assays.

resultsCompared to controls, ADHD model mice exhibited: Increased total distance in OFT, Decreased recognition index in NOR, Reduced context- and cue-related freezing time in FC and Attenuated theta oscillation power in the prefrontal cortex. RNA sequencing revealed significant enrichment of the PI3KC3 pathway and autophagy-related genes. ADHD model mice showed upregulated autophagy-related protein expression, elevated LC3II/I ratio, increased autophagosomes, and accumulated abnormal organelles in the mPFC. TH-positive neurities and PSD95-positive puncta were significantly reduced in the mPFC. 3-MA treatment partially reversed these alterations.

conclusionCognitive and memory impairments in the mPFC due to ADHD are correlated with autophagy, and these impairments might be alleviated by 3-MA.

Indexed as

3-methyladenineAttention-Deficit/Hyperactivity disorderAutophagyCognitive and memory dysfunctionMedial prefrontal cortex

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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.