Journal Article

DZNE-2026-00551

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Neuid: A Novel Neuron-Enriched LncRNA that Connects Epigenetic Gene Silencing to Alzheimer's Disease.

Pradhan, R. (First author)DZNE* ; Petrovic, Z. ; Sakib, S.DZNE* ; Schröder, S.DZNE* ; Krüger, D. M.DZNE* ; Pena, T.DZNE* ; Diniz, E.DZNE* ; Burkhardt, S.DZNE* ; Schütz, A.-L.DZNE* ; Gisa, V.DZNE* ; Grzadzielewska, I.DZNE* ; Toischer, K. ; Stein, T. D. ; Blusztajn, J. K. ; Delalle, I. ; Radulovic, J. ; Sananbenesi, F.DZNE* ; Fischer, A.Extern*

2026
Wiley-VCH Weinheim

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Please use a persistent id in citations: doi:10.1002/advs.202514972

Abstract: The increasing evidence that non-coding RNAs can become deregulated during pathogenesis is dramatically expanding the space for drug discovery beyond the protein-coding genome. Long noncoding RNAs (lncRNAs) are emerging as key regulators of cellular function, yet most remain uncharacterized. Here, we identify a previously unstudied lncRNA, which we named Neuronal Identity (Neuid), a conserved, brain-enriched transcript expressed in neurons. Neuid is downregulated in the brains of Alzheimer's disease (AD) patients. Mechanistically, Neuid maintains neuronal identity by repressing developmental and glial genes via interaction with the PRC2 subunit EZH2 and regulation of H3K27me3. Knockdown of Neuid disrupts this repression, leading to impaired neuronal activity and memory formation. Importantly, CRISPRa-mediated Neuid overexpression restores neuronal function in Aβ42-treated neurons. These findings identify NeuID as a critical regulator of neuronal plasticity and position it as a promising therapeutic target for AD.

Keyword(s): Alzheimer Disease: genetics (MeSH) ; Alzheimer Disease: metabolism (MeSH) ; RNA, Long Noncoding: genetics (MeSH) ; RNA, Long Noncoding: metabolism (MeSH) ; Neurons: metabolism (MeSH) ; Humans (MeSH) ; Gene Silencing (MeSH) ; Epigenesis, Genetic: genetics (MeSH) ; Animals (MeSH) ; Mice (MeSH) ; Enhancer of Zeste Homolog 2 Protein: genetics (MeSH) ; Enhancer of Zeste Homolog 2 Protein: metabolism (MeSH) ; Brain: metabolism (MeSH) ; brain ; epigenetics ; long‐non‐coding RNA ; neurodegeneration ; non‐coding RNA ; RNA, Long Noncoding ; Enhancer of Zeste Homolog 2 Protein

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Contributing Institute(s):

1. Epigenetics and Systems Medicine in Neurodegenerative Diseases (AG Fischer)
2. Clinical Dementia Research (Göttingen) (Clinical Dementia Research (Göttingen))
3. Bioinformatics and Genome Dynamics Core (Göttingen) (Bioinformatics Unit (Göttingen))
4. Genome Dynamics in Neurodegenerative Diseases (AG Sananbenesi)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)
2. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

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