Evidence map›Paper›PMID 41882255›Full record

ArticleMolecular psychiatry2026

The dynamic impairment of synaptic transmission in the PCx-IL engram circuit contributes to early olfactory memory decline in Alzheimer's disease.

Yan Yan, Da Song, Guangfei Li, Junjie Li, Yuanhong Tang, Danyang Li, Jian Mao, Hui Li, Xiaoyun Liu, Ding Yu and 11 more

Abstract read
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In one paragraph

Article in Molecular 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.

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0citing papers in PubMed
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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.

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

21 authors.

Yan Yan *International University Park Road, Dayun New Town, Longgang District, Shenzhen MSU-BIT University, Shenzhen, China.
Da Song *Key Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Guangfei Li *Department of Biomedical Engineering, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Junjie LiGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Children and Adolescents' Health and Diseases, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yuanhong TangKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Danyang LiKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Jian MaoFlavour Science Laboratory, Beijing Life Science Academy (BLSA), Beijing, 102209, China.ORCID http://orcid.org/0000-0002-2732-3403
Hui LiInternational University Park Road, Dayun New Town, Longgang District, Shenzhen MSU-BIT University, Shenzhen, China.
Xiaoyun LiuDepartment of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Ding YuDepartment of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Fangfang MaDepartment of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Yayan PangGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Children and Adolescents' Health and Diseases, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yue JinKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Yujun DengKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Yunjie QiuKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Zhenzhen QuanKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.ORCID http://orcid.org/0000-0002-2557-0371
Junjun NiKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.ORCID http://orcid.org/0000-0001-8486-8146
Yong ChengKey Laboratory of Ethnomedicine for Ministry of Education, Center on Translational Neuroscience, College of Life and Environmental Sciences, Minzu University of China, Beijing, China.ORCID http://orcid.org/0000-0002-7529-4408
Zhe WangAdvanced Innovation Center for Human Brain Protection, Capital Medical University; The National Clinical Research Center for Geriatric Disease, Xuanwu Hospital, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0003-4255-6763
Zhifang DongGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Children and Adolescents' Health and Diseases, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. zfdong@cqmu.edu.cn.ORCID http://orcid.org/0000-0002-3411-7923
Qing HongInternational University Park Road, Dayun New Town, Longgang District, Shenzhen MSU-BIT University, Shenzhen, China. hqing@smbu.edu.cn.ORCID http://orcid.org/0000-0003-2820-450X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82371446
6 · The paper itself

Abstract

Olfactory dysfunction has emerged as a promising target for the early diagnosis and treatment of Alzheimer's disease (AD). However, the mechanisms underlying neural circuit disruption associated with olfactory dysfunction in AD remain poorly understood. We conducted single-cell RNA sequencing (RNA-seq) and ex vivo electrophysiological studies to determine the link between olfactory memory in AD and dynamic synaptic transmission disorders in PCx-IL engram cell circuits. Clinical functional magnetic resonance imaging (fMRI) data revealed that connectivity between the piriform cortex (PCx) and the infralimbic cortex (IL) was impaired during the early mild cognitive impairment (MCI) stage of AD. Optogenetic stimulation of IL-projecting PCx engram neurons successfully improved olfactory memory retrieval in 5xFAD mice. In addition, single-cell RNA sequencing was employed to investigate the mechanisms of damage in IL engram cells, which revealed increased glutamate expression and impaired synaptic function as key alterations. Guided by single-cell sequencing data, we analyzed glutamatergic synaptic transmission in the PCx-IL engram cell circuit in 5xFAD mice. These results indicated dynamic impairments in AMPA receptor-associated synaptic transmission within this circuit. Optical long-term potentiation (LTP) of synaptic transmission restored directional engram synaptic transmission and prevented olfactory memory decline. Therefore, dynamic impairment of synaptic transmission in the PCx-IL engram cell circuit underlies the early decline in olfactory memory in AD. Impairment of PCx-IL functional connectivity may represent a new target for the diagnosis and treatment of early-stage AD.

Indexed as

Alzheimer DiseaseSynaptic TransmissionAnimalsCognitive DysfunctionDisease Models, AnimalFemaleHumansLong-Term PotentiationMagnetic Resonance ImagingMaleMemoryMemory DisordersMiceMice, Inbred C57BLMice, TransgenicNeurons

Identifiers

PMID41882255

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