This presentation is on the advancements in psychiatry regarding translational neuroscience.

1. Presenter: Dr. AISWARYA RENIL
Moderator: Dr. Major Kumar

2.  .The term translational can be characterized as the process of obtaining benefit for patients by
converting scientific discoveries from preclinical research into clinical applications, with the goal
of improving health para- meters, consequently decreasing morbidity and mortality.
 Translational research also refers to those activities conducted to bridge the gap between drug
discovery in pre clinical models and drug development in humans.
 It has been used to refer to the entire enterprise of medicine: “from bench to bedside and from
bedside to bench
 Translational research seeks to produce more meaningful, applicable results that directly
benefit human health.
 Its goal is to translate (move) basic science discoveries more quickly and efficiently into practice.

3.  Translational neuroscience is a fascinating field that aims to bridge the gap
between fundamental scientific research and its practical application in treating
neurological disorders.
 It focuses on applying discoveries made in the laboratory to develop new therapies
and interventions for patients in a clinical setting.
Caitlin Davies, Olivia K L Hamilton, Monique Hooley, Tuula E Ritakari, Anna J Stevenson, Emily N W Wheater, Translational neuroscience: the state of the nation (a PhD student perspective), Brain
Communications, Volume 2, Issue 1, 2020, fcaa038,

4.  Translational neuroscience is a step before clinical neuroscience.
 In order from least to most clinical:
 Exploratory ->Translational -> Clinical
 Think of the magnifying glass getting closer with each step
 It is more focused on developing tools or frameworks/theories/etc. that will show
promise in a clinical realm, but the research topics are not developed enough to
warrant clinical studies (yet).

5.  Translational research in psychiatry involves the development of useful animal behavioral models of psychiatric disorders and
preclinical in vitro/vivo studies using brain cells.
 When validated, these new agents are tested in phase 1 translational studies (pharmacokinetics, dose and tolerability), which together
with clinical trial phase 2 studies (proof of concept trial evaluating efficacy).
 These two step use new tools and other technological advances (e.g. bioinformatics), also searching for potential biomarkers
(preferentially in early phases).
 The next step in the translational paradigm involves the approval in phase 3 and posterior application of new public health policies
focusing on prevention and early intervention in mental disorders.

7.  At the core of translational neuroscience is the ‘wet’ laboratory research, which
aims to understand underlying disease mechanisms and how they can be targeted
for therapeutic purposes.

 One explanation for why this research has struggled to translate into the clinic may
be the difficulty in studying the human brain in a laboratory setting.
 This is presently done using a medley of models from animals to human cells and
post-mortem tissue; however, each is subject to inherent limitations in their
availability, complexity and ability to recapitulate human brain function

8.  One of the most commonly used models for preclinical research is small rodents,
mainly mice and rats. However, whilst animal models are indispensable for
studying the intact, live nervous system, rodents lack the complexity of the human
brain and do not fully recapitulate complex human disease.

9.  Cell Culture Facilities: These labs focus on growing and maintaining neuronal or glial cells in
vitro. Researchers can study cellular processes, drug responses, and disease mechanisms in a
controlled environment.
 Animal Model Facilities: Wet labs often utilize animal models, such as mice or rats, to study
neurological diseases and test potential treatments.These labs may involve techniques like
surgery, behavior testing, and histological analysis.
 Electrophysiology Labs:These labs investigate the electrical properties of neurons and neural
circuits.Techniques like patch-clamp recording and multi-electrode array recording are used to
study synaptic transmission, neural firing patterns, and network activity.
 Molecular Biology Labs: Molecular techniques like PCR,Western blotting, and gene editing
(e.g., CRISPR/Cas9) are essential for studying gene expression, protein function, and genetic
mutations associated with neurological disorders.

10.  Dry labs include directly biological concepts, such as the analysis of ‘omics’ for
target intervention and medical imaging for diagnostics.
 Another area of dry lab research that has greatly expanded in recent years, and
offers a promising avenue for translational outcomes, is the analysis of data
accrued through large-scale cohort studies and biobanks.
 DNA sequencing, brain scans, cognitive tests and output from wearable devices are
just some of the data gathered by these studies, all of which can be analysed with
the aim of delineating disease aetiologies or identifying biomarkers.

11.  Neuroimaging Centers: Neuroimaging facilities utilize techniques like MRI, fMRI,
PET, and EEG to visualize brain structure and function in both healthy individuals
and patients with neurological conditions
 Bioinformatics and Computational Neuroscience: Dry labs focus on analyzing
large datasets generated from experiments in wet labs. Bioinformatics tools are
used to study genomics, transcriptomics, and proteomics data to identify
biomarkers, genetic risk factors, and therapeutic targets for neurological diseases.
 Systems Biology Modeling: Computational models are used to simulate neural
circuits, synaptic plasticity, and brain dynamics.These models help researchers
understand how alterations at the molecular and cellular levels contribute to
neurological disorders and how interventions may restore normal function.

12.  Clinical Trials and Epidemiology Research:
Dry labs in translational neuroscience design and analyze clinical trials to test the safety and
efficacy of new treatments for neurological disorders.
Epidemiological studies examine patterns of disease occurrence and risk factors in
populations to inform prevention and treatment strategies.
 Drug Discovery andVirtual Screening:
Using computational approaches, researchers can predict the interactions between potential
drug candidates and their molecular targets.
Virtual screening techniques help identify lead compounds for further testing in wet lab
experiments.
 Data Mining and Knowledge Integration: Dry labs integrate data from diverse sources,
including clinical records, genetic databases, and literature repositories, to gain insights
into disease mechanisms and treatment responses. Data mining techniques uncover
hidden patterns and associations that may inform translational research efforts

13.  FDA definition
 “a defined characteristic that is measured as an indicator of
normal biological processes, pathogenic processes or
responses to an exposure or intervention.”

14.  BPAD
 In bipolar disorder (BD), the SNP rs17026688 in the gene encoding glutamate
decarboxylase-like protein 1 (GADL1) has been associated with the response to
lithium in Chinese patients
 This SNP (single nucleotide polynorphism) has been related to immune
dysfunctions in BPAD patients, such as higher percentages of totalT cells, CD4+T
cells, activated B cells and monocytes. Besides, treatment of BPAD patients-
derived peripheral blood mononuclear cells (PBMCs) with lithium in vitro increases
the immune response (CD4+ cells).
 These findings suggest that the immune imbalance might not only be a biomarker
for diagnosis but also a biomarker of the disease progression and therapeutic
response in BPAD

15.  The transcriptome is defined as the complete set of all RNA molecules in one cell or
a population of cells at a specific developmental stage or physiological condition.
 Thus, transcriptome is dynamic and reflects the cellular state.
 Measuring the expression of an organism’s genes as a snapshot in different tissues,
conditions, or time points provides information on how genes are regulated and
would contribute to a better understanding of human diseases and their
pharmacological treatment, allowing to identify potential therapeutic biomarkers
when variations in treatment outcomes occur.
 Transcriptomics studies identified that the efficacy of antidepressants is related to
gene expression changes at transcriptome-wide scale.

16.  Alterations of MMO28 and KXD1 genes encoding for matrix metallopeptidase 28 and
KxDL motif-containing protein 1, respectively, were associated with better response to
nortriptyline in depressive patients.
 This data could contribute to improve the characterization of the molecular pathways
underlying the efficacy of antidepressants.

 In addition, a clinical study associated new miRNAs (miR-146a-5p, miR-146b-5p, 399 miR-
24-3p and miR-425-3p) with the effectiveness of antidepressant drugs such as duloxetine,
escitalopram, and nortriptyline, in patients with MDD.

17.  Another study revealed that MDD (major depressive disorder) patients responders to
antidepressant treatment present a significant reduction of miR-1202 baseline levels
compared to non-responders.
 Moreover, miR-1202 increases as the efficacy of the antidepressant treatment is observed.
 Besides, a total of 25 miRNAs have been modified in the amygdala of rats exposed to the
learned helpless animal model of depression being the miR-128-3p the most affected.

18.  Other example of the potential role of these biomarkers in neuropsychiatry is a genome-
wide expression study in patients who met the DSM-V criteria for methamphetamine
dependence.
 The results revealed that treatment with topiramate significantly modified the gene
expression of specified genes GRINA, PRKACA, PRKCI, SNAP23 andTRAK2 involved in
severe pathways underlying drug addiction and other relevant physiological functions,
including neuronal function/synaptic plasticity, signal transduction, cardiovascular
function, and inflammation/immune response.
 Likewise, the microRNA-124 (miR-124) and microRNA-181 (miR-181) were pointed out as
potential biomarkers for cocaine use disorder (CUD).
 The study revealed that these two microRNAs were upregulated in the blood samples of
females CUD compared with healthy female controls.

19.  Proteomics approaches using blood, plasma or serum constitutes a highly desired
method for biomarker profiling of psychiatric disorders, due to the fact that these
biological samples are used for routine diagnostic analyses in clinical practice,
making easier to obtain samples.
 Besides, in neuropsychiatry, the cerebrospinal fluid (CSF) is a sample of particular
interest for the identification of potential proteomic biomarkers due to its
proximity to the brain.
 Although its collecting is very complex, due to the invasive procedure involved, it
contains much less proteins than plasma.
 Thus, the “buffering” of protein composition is much weaker and tend to lead in a
reduction of chances to identify potential proteomic biomarkers.

20.  Proteome studies carried out in blood plasma, serum and postmortem brain tissue from
SCZ patients identified alterations in proteins that play a significant role in neuronal
transmission and synaptic function, calcium homeostasis and signalling, energy
metabolism, oxidative stress, cytoskeleton and in immune system and inflammation.
These proteins have been proposed as biomarker candidates for prognosis, diagnosis, and
medication monitoring in SCZ .
 One of these proteins is zinc finger protein 729, that was found significantly down-
regulated in patients with SCZ compared to healthy individuals and patients diagnosed
with depression or BD.
 Another example is the study that showed reduced plasma levels of glia maturation factor
beta (GMF-β), the brain-derived neurotrophic factor (BDNF), and the 115-kDa isoform of
the Rab3 GTPase-activating protein catalytic subunit (RAB3GAP1) in SCZ patients.
 These biological markers have been proposed as potential biomarkers in this pathology.

21.  Besides, the acetyl-l-carnitine (LAC) has been proposed as a proteomic biomarker
in MDD.
 LAC plays an important role in several behavioral features.
 The reduction of LAC concentrations was associated with abnormal hippocampal
glutamatergic function and plasticity.
 Such alterations suggested that the degree of LAC deficiency was directly
proportional with the severity, the age of MDD onset, and the clinical history of
treatment-resistant depression (TRD).
 These findings suggest that LAC may be useful as a diagnostic and prognosis
biomarker for MDD.

22.  Recently, neurofilaments light chains (NF-L) have been proposed as potential biomarkers
for neuronal damage in certain psychiatric diseases.
 In the plasma of female patients affected by anorexia nervosa, levels of NF-L were
significantly elevated, being associated with the neuronal damage observed in AN
patients, that partially normalizes with weight recovery.
 Interestingly, a reduction of NF-L has been identified in the hippocampus of rodents
exposed to an animal model of depression (inescapable stress).
 In this study, treatment with valproic acid reduces depressive-like behavior and reverses
NF-L reduction.
 Besides, elevated concentrations of NF-L have been observed in the CSF of BD patients.
 Authors demonstrated that there is a positive correlation between CSF NF-L levels and the
response to antipsychotics and lithium.
 However, another prospective study failed to observe any association between the high
baseline NF-L levels in CSF and clinical outcomes in BD.
NFL
•Anorexia nervosa
•bpad
Depression

23.  This technology focuses on the presence of small molecules metabolites in various complex
matrices like CSF, blood, urine, saliva and other human fluids.
 Changes in metabolome are the consequence of the interaction between lifestyle, environmental,
genetic, developmental and pathological factors.
 Consequently, metabolomics are of particular interest because it captures the dynamic nature of
the disease, measure the final products produced by complex interactions between proteins,
signaling cascades and cellular environments.
 Metabolomics biomarkers are not characterized by one single metabolite. Rather, they are a set of
correlated metabolites defining a specific state of disease or the response to a clinical or
pharmacological intervention.

24.  Urinary metabolomics have been proposed to be potential useful tools for the Identification of
pathways that may be involved in the mechanism of action of specific treatments.
 Urinary metabolites were identified in children with autism spectrum disorder treated with
sulforaphane, a supplement that significantly improved the social responsiveness.
 Recently, a study conducted in patients with symptoms of depression, tried to found a
predictor or a biological correlation of depression recovery after the administration of certain
antidepressants including escitalopram, bupropion-escitalopram or venlafaxine-mirtazapine
combinations.
 An increase of phosphatidylcholine C38:1 baseline plasma concentrations was associated with
poorer outcome in patients.
 In contrast, an increased ratio in hydroxylated sphingomyelins after 8 weeks of treatment was
linked to symptoms recovery .

25.  Epigenetics is the study of how your behaviors and environment can cause changes that
affect the way your genes work.
 Epigenetic biomarkers have been pointed out as potential biomarkers for guiding
treatment.
 Thus, antipsychotic drugs, such as olanzapine, induced DNA methylations alterations
through the brain in SCZ patients, changes related with its efficacy.
 For instance, reduced response to antidepressants has been associated with the absence of
methylation at a specific CpG site in exon 4 of BDNF in MDD patients.
 Consequently, BDNF exon 4 methylation and circulating BDNF protein levels may be used
together as a predictive tool to personalize treatment of MDD

26.  More interestingly, histone deacetylases (HDAC), that have been demonstrated to control
epigenetic programming associated with the modulation of behavior and cognition, appears
to be crucial for reversing dysfunctional epigenetic regulation induced by early life events
exposure in preclinical models .
 Additional studies have supported the potential role of HDAC as promising new therapeutic
targets for the treatment of MDD.
 In this context, HDAC inhibitors, alone or in combination with current antidepressant drugs, are
currently being explored .
 Altogether, epigenetic studies highlight the importance of epigenetic mechanisms on
controlling genes or gene complexes

27.  HDAC inhibitors have been highlighted as a novel category of anti-cancer drugs.To date,
four HDAC inhibitors,
1. Vorinostat,
2. Romidepsin,
3. Panobinostat, and
4. Belinostat,
have been approved by the United States Food and Drug Administration.

28. Zanardi, R., Prestifilippo, D., Fabbri, C., Colombo, C., Maron, E., & Serretti, A. (2021). Precision psychiatry in clinical practice. International Journal of Psychiatry in Clinical
Practice, 25(1), 19–27. https://doi.org/10.1080/13651501.2020.1809680

29. Berk, M. (2023). Biomarkers in psychiatric disorders: status quo, impediments and facilitators. World
Psychiatry: Official Journal of the World Psychiatric Association (WPA), 22(2), 174–176.
https://doi.org/10.1002/wps.21071

30.  An animal model can be viewed as an experimental paradigm developed for the
purpose of studying a given phenomenon found in humans.
 Animal models for a complete syndrome of a psychiatric disorder are un- likely to
be possible either conceptually or practically.
 Thus, although there are no complete animal models of addiction, anxiety, or
depression, animal models do exist for many elements of the syndrome.

31.  One of the most commonly used models for preclinical research is small rodents,
mainly mice and rats.
 However, whilst animal models are indispensable for studying the intact, live nervous
system, rodents lack the complexity of the human brain and do not fully recapitulate
complex human disease.
 A promising development for the field of translational neuroscience has been the
advent of human induced pluripotent stem cell technology.This has been gaining
popularity as a disease model, as it allows researchers to study dynamic disease
processes in live human cells with practically unlimited material.

32. Shrew
Rat
Mice

33.  Forced swim test (in rats and mice)
 Tail suspension test
 Learned helplessness (in rats and mice)
 Olfactory bulbectomy (in rats and mice)
 Differential reinforcement of low rates of responding (72 seconds;
in rats)
 Maternal deprivation
 Neonatal clomipramine treatment (in rats and mice)
 Social stress (in shrews)
 Chronic mild stress Agonistic behavior
 Flinders sensitive rats

34.  The Flinders Sensitive Line (FSL) of rats, developed as a line of rats with
behavioral supersensitivity to diisopropyl fluorophosphates, a cholinesterase inhibitor, has
been used as a rat model of depression.
 Utilizing the Flinders Sensitive Line rat as an animal model of major depression genetic
risk, the authors characterized interactions between genetic risk, social isolation, and
antidepressant treatment on behavioral and biochemical outcome measures of relevance
to treatment resistant depression.
 They observed combined effects of genetic vulnerability in Flinders Sensitive Line rats,
interacting with social isolation, resulting in behavioral and biochemical measures more
resistant to antidepressant treatment.

35.  Obsessive-compulsive (OC) traits demonstrate considerable heritability, indicating that
genetic factors play an important role in their pathogenesis. Although it is not feasible to
assess obsessive-like mental experiences in a non-human animal, it is possible to observe
repetitive and compulsive-like behaviors—occurring either spontaneously or induced by
some experimental manipulation.
 Mitra and Bult-Ito review studies of a mouse reports important effects of gonadal hormones
and the oxytocinergic system on compulsive-like behavior in female mice, providing clues
on the physiological underpinnings of OC symptoms associated with the female
reproductive cycle.
 These mouse lines present an excellent opportunity to investigate how interactions
between genetic liability, physiological state, and environmental factors contribute to the
pathogenesis of obsessive-compulsive symptoms.

36.  Anorexia nervosa (AN) is a potentially fatal illness presenting with suboptimal
psychological and behavioral therapies, while pharmacological treatments are lacking in
therapeutic efficacy.
 AN has strong metabolic and psychiatric origins, suggesting its reconceptualization as a
metabo-psychiatric disorder.
 Zhang and Dulawa posit that, despite limitations such as an inability to mimic certain
psychological constructs of the disorder, the activity-based anorexia (ABA) paradigm
allows the reconceptualization of AN in this manner.
 In so doing the authors highlight how modern circuit-dissecting neuroscience techniques
may be invaluable in identifying metabo-psychiatric mechanisms that regulate ABA, as
well as genetic variants and gene pathways in AN.This will aid in identifying novel targets
and treatment strategies for AN.

37.  Neuroimaging techniques enable the visualisation of the anatomy, function and
pharmacology of the brain.
 Some techniques, such as computed tomography (CT), electroencephalography
(EEG) and structural magnetic resonance imaging (sMRI), are well established in
clinical practice, whereas more contemporary techniques, such as functional MRI
(fMRI) and diffusion tensor imaging (DTI), have yet to show their full translational
potential.
1. Martinelli C, Shergill SS. Everything you wanted to know about neuroimaging and psychiatry, but were afraid to ask. BJPsych Advances. 2015;21(4):251–60.
doi:10.1192/apt.bp.114.013763

38.  Structural magnetic resonance imaging (sMRI)
 explore the effects of medication on brain structures
 connect psychiatric and biochemical abnormalities to changes in structure for a
better understanding of pathophysiology.
 Functional MRI
 identify brain networks underlying specific psychological functions
 test cognitive models of illnesses
 examine the functional connectivity across different regions of the brain.
1. Martinelli C, Shergill SS. Everything you wanted to know about neuroimaging and psychiatry, but were afraid to ask. BJPsych Advances. 2015;21(4):251–60.
doi:10.1192/apt.bp.114.013763

40.  Electro encephalography (EEG)
 Magneto Encephalography(MEG)

41.  Schizophrenia
Series of fMRI studies has helped to elucidate the formation of hallucinations in
schizophrenia, demonstrating that both speech generation areas and speech
perception areas are active during auditory hallucinations and that mechanistic
treatments such as transcranial direct current stimulation (tDCS) or repetitive
transcranial magnetic stimulation (rTMS) can be used to modulate brain activity in
these regions and improve symptoms.
1. Martinelli C, Shergill SS. Everything you wanted to know about neuroimaging and psychiatry, but were afraid to ask. BJPsych Advances. 2015;21(4):251–60.
doi:10.1192/apt.bp.114.013763

43.  PET imaging has shown increased aberrant activity in the SCG of depressed people
and of healthy individuals retrieving sad autobiographical memories.Also, a decrease
in SCG activity has been observed after successful treatments employing various
modalities
 Neuroimaging data have identified the subcallosal cingulate gyrus (SCG) as a
candidate structure for deep brain stimulation (DBS).
1. Martinelli C, Shergill SS. Everything you wanted to know about neuroimaging and psychiatry, but were afraid to ask. BJPsych Advances. 2015;21(4):251–60.
doi:10.1192/apt.bp.114.013763

44.  Neuroimaging studies have influenced the categorisation of disordered gambling, recently
moved from the category of impulse disorders to that of addiction in the latest version of the
DSM-5 .
 This reclassification rests on various evidence of shared features between drug addiction and
gambling disorder including similar involvement of dopamine-mediated reward circuits, as
demonstrated by neuroimaging.
•The dopaminergic pathway mostly involved in reward is the so-
called mesolimbic system, which is formed by projections of
•midbrain dopamine neurons of the ventral tegmental area
(VTA) to the striatum,
•prefrontal cortex,
• amygdala,
•hippocampus, and many other structures of the limbic system.

45. 1. Identification of aTarget:
2. Translating to HumanTrials: If the preclinical studies show
promising results, researchers can proceed with human trials to
evaluate the safety and efficacy of the potential treatment in a
controlled clinical setting.
3. Clinical Research: Clinical trials are conducted to test the
treatment’s effectiveness on a larger population.These trials
provide critical data that helps determine whether the treatment
should be approved for widespread clinical use.
4. Application in Patient Care: If the treatment proves successful in
clinical trials, it can be implemented as a part of standard
medical practice, benefiting patients suffering from the disease .

46. Precision medicine, as a kind of personalised medicine, facilitating decision-making before choosing a
particular medication, takes into account the patients’
 history and circumstances of the disease,
 symptom profile,
 gender, weight, known metabolic abnormalities,
 Substance use
 Other environmental factors
 previous therapeutic adherence
 frequent therapeutic drug monitoring
 measurable biomarkers, ie, indicators of normal biological processes, pathogenic processes, or
responses to the exposure or intervention..
 Neuroimaging etc
Zanardi, R., Prestifilippo, D., Fabbri, C., Colombo, C., Maron, E., & Serretti, A. (2021). Precision psychiatry in clinical practice. International Journal of Psychiatry in Clinical
Practice, 25(1), 19–27. https://doi.org/10.1080/13651501.2020.1809680

47. Data gathering
Treatment
decisions
Monitoring &
prevention
Standard care
•Clinical: interview,
observation,
questionaries
•Environmental: Trauma
history, life stressors
• Biological: Blood work
Choose among 1st line
evidence-based medication
therapies using:
•Clinical experience
•Side effect profiles
•Patient preference
•Family history of response
Follow-up every 1-3
months
Precision psychiatry
•All above
•Biological:
pharmacogenomics,
biomarkers, inflammatory
markers etc
•functional MRI or other
neuroimaging
Treatments based on
matching to
individualized
profiles
•As above
• Monitor using real-time
data collection (é.g.,
smartphones)
•intervene before relapse

49.  1. Complexity of psychiatric disorders: Psychiatric disorders are multifaceted conditions influenced
by genetic, environmental, and social factors.Translating basic neuroscience findings into clinical
applications for such complex disorders can be challenging.
 2. Heterogeneity of patient populations: Patients with psychiatric disorders often present with
diverse symptoms and treatment responses, making it difficult to generalize findings from
translational research to all individuals with the same diagnosis.
 3. Lack of biomarkers: Unlike some medical conditions where biomarkers indicate disease presence
or progression, psychiatric disorders often lack objective biomarkers, hindering the development of
precise diagnostic tools and targeted treatments.

50.  4. Ethical considerations:Conducting translational research in psychiatry raises ethical concerns
regarding patient consent, privacy, and the potential misuse of neuroscientific findings, particularly
those related to brain imaging and genetics.
 5.Translation gap:There is often a gap between basic neuroscience research and clinical practice,
where promising findings from the laboratory fail to translate into effective treatments for
patients.
 6. Reproducibility issues: Replicating findings from basic neuroscience studies in clinical settings
can be challenging due to variations in experimental conditions, sample sizes, and methodologies,
leading to difficulties in validating translational research findings.
 Addressing these limitations requires interdisciplinary collaboration, innovative research
methodologies, and a nuanced understanding of the complex interactions between biological,
psychological, and social factors underlying psychiatric disorders.

51. 1. 1. Martinelli C, Shergill SS. Everything you wanted to know about neuroimaging and psychiatry, but were
afraid to ask. BJPsych Advances. 2015;21(4):251–60. doi:10.1192/apt.bp.114.013763
2. Machado-Vieira, R. (2012).Tracking the impact of translational research in psychiatry: state of the art and
perspectives. Journal ofTranslational Medicine, 10(1), 175. https://doi.org/10.1186/1479-5876-10-175
3. Marková, I. S. (2018).Translational neuroscience and psychiatry:A conceptual analysis. Journal of Evaluation in
Clinical Practice, 24(4), 791–796. https://doi.org/10.1111/jep.12914
4. Veenstra-VanderWeele, J., O’Reilly, K. C., Dennis, M.Y., Uribe-Salazar, J. M., & Amaral, D. G. (2023).
Translational neuroscience approaches to understanding autism.The American Journal of Psychiatry, 180(4),
265–276. https://doi.org/10.1176/appi.ajp.20230153
5. Line of rats, a rat model of depression, has elevated brain glucose utilization when compared to normal rats
and the Flinders Resistant Line of rats. Neurochem Int. 2009 Dec;55(7):655-61. doi:
10.1016/j.neuint.2009.06.011. Epub 2009 Jun 26. PMID: 19560506.
6. Vecera CM, Fries GR, Shahani LR, Soares JC, Machado-Vieira R. Pharmacogenomics of Lithium Response in
Bipolar Disorder. Pharmaceuticals (Basel). 2021 Mar 24;14(4):287. doi: 10.3390/ph14040287. PMID: 33804842;
PMCID: PMC8063790.
7. Caitlin Davies, Olivia K L Hamilton, Monique Hooley,Tuula E Ritakari, Anna J Stevenson, Emily NWWheater,
Translational neuroscience: the state of the nation (a PhD student perspective), Brain Communications,
Volume 2, Issue 1, 2020, fcaa038,

52.  Anticevic,A., Krystal, J. H., & Barch, D. M. (2013).Translational cognitive neuroscience of schizophrenia:
Bridging neurocognitive and computational approaches toward understanding cognitive deficits. In P. D.
Harvey (Ed.), Cognitive impairment in schizophrenia:Characteristics, assessment and treatment (pp. 193–230).
Cambridge University Press.

53.  Thank you