He is former scientific director of the Division of Intramural Research Programs at the National Institute of Mental Health,[3] having also served as member of the Board of Regents of the University of Minho, Portugal.

He arrived in the United States in 1978, attended Rutgers University, where he studied biology and philosophy and worked in the Drosophila laboratory of William Sofer.

[5] It was also in Utah, while working with Mario Capecchi, that he had the idea of bringing the newly developed mouse gene targeting approaches [6] to studies of memory.

After attending a Society for Neuroscience symposium (Toronto, 1988), organized by John Lisman on mechanisms of hippocampal plasticity, Silva decided to study hippocampal-dependent memory formation.

[1][2] The two articles he published in Science as a post-doctural fellow in Susumu Tonegawa's laboratory were the first to combine molecular genetic techniques with electrophysiological analyses and behavioral studies.

For example, Rousudan Bourtchuladze led a project in the Silva laboratory that uncovered a role for the transcription factor CREB in the stability of hippocampal long term potentiation and long-term memory.

Additionally, UCLA's large and highly collaborative neuroscience community was an ideal environment for the interdisciplinary studies that characterized work in the Silva laboratory.

[18] This discovery, and a series of later studies in many laboratories worldwide, have demonstrated the surprising efficacy of adult interventions in reversing cognitive phenotypes in animal models of neurodevelopmental disorders.

[25] Weidong Li and Steven Kushner led a team in the Silva lab that developed a treatment for the cognitive deficits associated with an animal model of Neurofibromatosis type I (NF1).

[32][33] A team led by Dan Ehninger in the Silva lab also showed that rapamycin, an FDA approved inhibitor of mTOR, can reverse the late-LTP deficits and learning impairments they discovered in an animal model of Tuberous Sclerosis (Tsc2 heterozygous mice).

All together, these findings make a compelling case that adult treatments may be effective at reversing behavioral cognitive and psychiatric symptoms associated with neurodevelopmental disorders such as NF1, TSC and schizophrenia.

[38] Frankland and colleagues in the Silva lab also used a combination of genetic, imaging and reversible lesion approaches to search for regions in the neocortex that are involved in remote memory.

[40][41] These studies indicated that unlike the hippocampus, prefrontal cortical regions, such as the anterior cingulate, have a critical role in remote, but not in recent memory retrieval.

These authors also showed that memory linking mechanisms are affected in the aging brain, and that manipulating excitability in a subset of neurons reverses these deficits.

"[48] In 2022 Yang Shen, Miou Zhou and colleagues in the Silva lab discovered that the delayed expression of the receptor CCR5 closes the window of time in which two memories can be linked.

[51][52][53] They propose that these maps of research findings would also be invaluable during experiment planning: Understanding more objectively the implications of the millions of neuroscience papers already published would allow neuroscientists to more clearly define what to do next.

To generate these maps, Landreth and Silva also developed a set of algorithms that formalize strategies neuroscientists use to determine the strength of evidence in their fields.