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Recent Research in Cerebellar Development and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 411

Special Issue Editor


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Guest Editor
Centre for Molecular Medicine and Therapeutics, British Columbia Children's Hospital Research Institute, Vancouver, BC V5Z 4H4, Canada
Interests: cerebellar development and anomalies; neurogenesis; neural migration; neural differentiation; microRNA

Special Issue Information

Dear Colleagues,

Cerebellum is involved in numerous functions from motor control to cognition and emotion. Although the cerebellum occupies about ten percent of brain volume, it contains ~ 80% of the brain's neurons, organized into dense cellular layers. This neuron-rich region is formed by two distinct germinal zones for GABAergic and glutamatergic lineages. The entire process of neural development—including neurogenesis, neuronal migration, and differentiation/maturation—is under precise molecular control, involving tightly regulated signaling, transcription, and epigenetic mechanisms in the cerebellum. Cerebellar cytoarchitecture and compartmentalization are established from embryonic through postnatal stages. A wide variety of congenital anomalies can affect this delicate brain region and are associated with developmental disabilities. Several genes implicated in congenital human cerebellar malformations have been identified and studied in mouse models. Moreover, exposure to toxic substances has profound effects on the developing cerebellum, resulting in neural cell death. In this issue, complementary human and mouse studies work synergistically to advance our understanding of the mechanisms governing cerebellar development and disease.

Dr. Maryam Rahimi-Balaei
Guest Editor

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Keywords

  • cerebellar development
  • cerebellum
  • neural development
  • neurogenesis
  • neuronal migration
  • cerebellar malformations

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Published Papers (1 paper)

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Research

27 pages, 14347 KB  
Article
Impact of Sema3A Interference on Cerebellum-Dependent Motor Associative Learning and Memory
by Geoffrey-Alexander Gimenez, Sarah Van Der Zwaag, Cynthia M. Geelen, Melissa Van Hemert, Jop Vreeken, Fred de Winter, Cathrin B. Canto, Daniela Carulli, Chris I. De Zeeuw and Joost Verhaagen
Int. J. Mol. Sci. 2026, 27(12), 5304; https://doi.org/10.3390/ijms27125304 - 11 Jun 2026
Viewed by 193
Abstract
Semaphorin 3A (Sema3A), a known axon chemorepulsive protein during development, is localised in perineuronal nets (PNNs) in the adult brain. PNNs are condensed aggregates of extracellular matrix molecules surrounding specific types of neurons, which regulate neuroplasticity and memory. However, the role of PNN-associated [...] Read more.
Semaphorin 3A (Sema3A), a known axon chemorepulsive protein during development, is localised in perineuronal nets (PNNs) in the adult brain. PNNs are condensed aggregates of extracellular matrix molecules surrounding specific types of neurons, which regulate neuroplasticity and memory. However, the role of PNN-associated Sema3A in these processes remains unclear. To address this topic, we investigated the contribution of Sema3A to cerebellum-dependent learning and memory in adult mice using the eyeblink conditioning (EBC) paradigm. We interfered with Sema3A signalling by employing: (i) a molecular approach, in which secreted Sema3A receptors (neuropilin-1 bodies) were expressed in the anterior interposed nuclei (AIN) via viral vector injection; and (ii) a genetic approach, using mutant mice with impaired Sema3A signalling (K108N mice). Mice expressing neuropilin-1 bodies showed reduced EBC performance at the beginning of the memory retention phase. However, increased inflammation was found in the AIN of these mice, challenging the interpretation of these findings. K108N mice showed enhanced EBC performance at the beginning of the memory retention phase. No synaptic structural changes were detected in the AIN of K108N mice at the end of the EBC paradigm. Based on our findings in K108N mice, constitutively altered Sema3A signalling is associated with subtle improvement in cerebellar memory. Full article
(This article belongs to the Special Issue Recent Research in Cerebellar Development and Disease)
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