ArticleTranslational neurodegeneration2026
Levetiracetam restores GABAergic function and network homeostasis following Vps35 deficiency in excitatory neurons.
Article in Translational neurodegeneration, 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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Abstract
backgroundAlzheimer's disease (AD) and related dementias (ADRDs) remain incurable, partly due to their complex and poorly understood pathogenic mechanisms. Loss of vacuolar protein sorting-associated protein 35 (VPS35), a core component of the retromer complex, has been implicated in AD and ADRDs. While Vps35 deficiency is known to increase amyloidogenesis by regulating its cargo proteins, such as APP and BACE1, the precise mechanism by which VPS35 dysfunction leads to cognitive impairment remains elusive. While neuronal VPS35 regulates trafficking and functions of multiple synaptic membrane proteins, such as postsynaptic glutamatergic and GABAnergic receptors and pre-synaptic vesicle protein SV2A, and Levetiracetam (LEV), an antiepileptic drug that improves cognition, interacts with the SV2A, exactly how LEV enhances cognition is still a matter of debate.
methodsGiven the abundant expression of VPS35 in pyramidal excitatory neurons, we generated a conditional knockout mouse model with Vps35 deletion from postnatal glutamatergic excitatory neurons (Vps35
resultsVps35 deletion did not disrupt the gross brain development but led to progressive cognitive decline beginning at three months of age. Electrophysiological analyses revealed earlier-onset hippocampal CA1 hyperexcitability, marked by depolarized resting membrane potentials and reduced Kir
conclusionsThese findings identify VPS35 in excitatory neurons as a critical factor for inhibitory synapse maintenance and network homeostasis. This study also highlights LEV as a potential therapeutic strategy for ADRDs through the preservation of GABAergic synapses.
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