ArticleHuman molecular genetics2015
A role for Kalirin-7 in corticostriatal synaptic dysfunction in Huntington's disease.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Photoactivated adenylyl cyclase in cortical astrocytes promotes synaptic potentiation and reveals alterations in Huntington's disease.iScience · 2025Article
- Restoration of CB1 receptor function in hippocampal GABAergic neurons rescues memory deficits in Huntington's disease models.Translational neurodegeneration · 2025Article
- Restoring endogenous Dlg4/PSD95 expression by an artificial transcription factor ameliorates cognitive and motor learning deficits in the R6/2 mouse model of Huntington's disease.Clinical epigenetics · 2025Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- BDNF and TRiC-inspired reagent rescue cortical synaptic deficits in a mouse model of Huntington's disease.Neurobiology of disease · 2024Article
- TYROBP/DAP12 knockout in Huntington's disease Q175 mice cell-autonomously decreases microglial expression of disease-associated genes and non-cell-autonomously mitigates astrogliosis and motor deterioration.Journal of neuroinflammation · 2024Article
- Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.Cellular and molecular life sciences : CMLS · 2023Article
- Roles of Rac1-Dependent Intrinsic Forgetting in Memory-Related Brain Disorders: Demon or Angel.International journal of molecular sciences · 2023Review
- P2YAging cell · 2023Article
- A pathogenic proteolysis-resistant huntingtin isoform induced by an antisense oligonucleotide maintains huntingtin function.JCI insight · 2022Article
- Altered m6A RNA methylation contributes to hippocampal memory deficits in Huntington's disease mice.Cellular and molecular life sciences : CMLS · 2022Article
- Differential Effects of Sevoflurane Exposure on Long-Term Fear Memory in Neonatal and Adult Rats.Molecular neurobiology · 2022Article
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Differential Transcriptome Profiling Unveils Novel Deregulated Gene Signatures Involved in Pathogenesis of Alzheimer's Disease.Biomedicines · 2022Article
- Quantification of Dendritic Spines Remodeling under Physiological Stimuli and in Pathological Conditions.International journal of molecular sciences · 2021Review
- Pharmacological Modulators of Small GTPases of Rho Family in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Article
- Synaptic RTP801 contributes to motor-learning dysfunction in Huntington's disease.Cell death & disease · 2020Article
- Modulation of dopamine DeLife · 2020Article
- Kalirin-7 contributes to type 2 diabetic neuropathic pain via the postsynaptic density-95/N-methyl-D-aspartate receptor 2B-dependent N-methyl-D-aspartate receptor 2B phosphorylation in the spinal cord in rats.American journal of translational research · 2020Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Cognitive dysfunction is an early clinical hallmark of Huntington's disease (HD) preceding the appearance of motor symptoms by several years. Neuronal dysfunction and altered corticostriatal connectivity have been postulated to be fundamental to explain these early disturbances. However, no treatments to attenuate cognitive changes have been successful: the reason may rely on the idea that the temporal sequence of pathological changes is as critical as the changes per se when new therapies are in development. To this aim, it becomes critical to use HD mouse models in which cognitive impairments appear prior to motor symptoms. In this study, we demonstrate procedural memory and motor learning deficits in two different HD mice and at ages preceding motor disturbances. These impairments are associated with altered corticostriatal long-term potentiation (LTP) and specific reduction of dendritic spine density and postsynaptic density (PSD)-95 and spinophilin-positive clusters in the cortex of HD mice. As a potential mechanism, we described an early decrease of Kalirin-7 (Kal7), a guanine-nucleotide exchange factor for Rho-like small GTPases critical to maintain excitatory synapse, in the cortex of HD mice. Supporting a role for Kal7 in HD synaptic deficits, exogenous expression of Kal7 restores the reduction of excitatory synapses in HD cortical cultures. Altogether, our results suggest that cortical dysfunction precedes striatal disturbances in HD and underlie early corticostriatal LTP and cognitive defects. Moreover, we identified diminished Kal7 as a key contributor to HD cortical alterations, placing Kal7 as a molecular target for future therapies aimed to restore corticostriatal function in HD.
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