@article{20154,
  abstract     = {In long-lived mammals, including humans, brain cell homeostasis is critical for maintaining brain function throughout life. Most neurons are generated during development and must maintain their cellular identity and plasticity to preserve brain function. Although extensive studies indicate the importance of recycling and regenerating cellular molecules to maintain cellular homeostasis, recent evidence has shown that some proteins and RNAs do not turn over for months and even years. We propose that these long-lived cellular molecules may be the basis for maintaining brain function in the long term, but also a potential convergent target of brain aging. We highlight key discoveries and challenges, and propose potential directions to unravel the mystery of brain cell longevity.},
  author       = {Hetzer, Martin W and Toda, Tomohisa},
  issn         = {1878-108X},
  journal      = {Trends in Neurosciences},
  number       = {9},
  pages        = {645--654},
  publisher    = {Cell Press},
  title        = {{Long-lived cellular molecules in the brain}},
  doi          = {10.1016/j.tins.2025.07.004},
  volume       = {48},
  year         = {2025},
}

@article{7957,
  abstract     = {Neurodevelopmental disorders (NDDs) are a class of disorders affecting brain development and function and are characterized by wide genetic and clinical variability. In this review, we discuss the multiple factors that influence the clinical presentation of NDDs, with particular attention to gene vulnerability, mutational load, and the two-hit model. Despite the complex architecture of
mutational events associated with NDDs, the various proteins involved appear to converge on common pathways, such as synaptic plasticity/function, chromatin remodelers and the mammalian target of rapamycin (mTOR) pathway. A thorough understanding of the mechanisms behind these pathways will hopefully lead to the identification of candidates that could be targeted for treatment approaches.},
  author       = {Parenti, Ilaria and Garcia Rabaneda, Luis E and Schön, Hanna and Novarino, Gaia},
  issn         = {1878-108X},
  journal      = {Trends in Neurosciences},
  number       = {8},
  pages        = {608--621},
  publisher    = {Elsevier},
  title        = {{Neurodevelopmental disorders: From genetics to functional pathways}},
  doi          = {10.1016/j.tins.2020.05.004},
  volume       = {43},
  year         = {2020},
}

@article{3805,
  abstract     = {The operation of neuronal networks crucially depends on a fast time course of signaling in inhibitory interneurons. Synapses that excite interneurons generate fast currents, owing to the expression of glutamate receptors of specific subunit composition. Interneurons generate brief action potentials in response to transient synaptic activation and discharge repetitively at very high frequencies during sustained stimulation. The ability to generate short-duration action potentials at high frequencies depends on the expression of specific voltage-gated K+ channels. Factors facilitating fast action potential initiation following synaptic excitation include depolarized interneuron resting potential, subthreshold conductances and active dendrites. Finally, GABA release at interneuron output synapses is rapid and highly synchronized, leading to a faster inhibition in postsynaptic interneurons than in principal cells. Thus, the expression of distinct transmitter receptors and voltage-gated ion channels ensures that interneurons operate with high speed and temporal precision.},
  author       = {Jonas, Peter M and Bischofberger, Josef and Fricker, Desdemona and Miles, Richard},
  issn         = {1878-108X},
  journal      = {Trends in Neurosciences},
  number       = {1},
  pages        = {30 -- 40},
  publisher    = {Elsevier},
  title        = {{Interneuron Diversity series: Fast in, fast out--temporal and spatial signal processing in hippocampal interneurons}},
  doi          = {doi:10.1016/j.tins.2003.10.010},
  volume       = {27},
  year         = {2004},
}

@misc{3142,
  author       = {Hippenmeyer, Simon and Kramer, Ina and Arber, Silvia},
  booktitle    = {Trends in Neurosciences},
  issn         = {1878-108X},
  number       = {8},
  pages        = {482 -- 488},
  publisher    = {Elsevier},
  title        = {{Control of neuronal phenotype: What targets tell the cell bodies}},
  doi          = {10.1016/j.tins.2004.05.012},
  volume       = {27},
  year         = {2004},
}