Review of th

Le

Use this grid or one of your own design to compare the methods & findings in the different texts you read to w

Our Working Statement of Purpose: After researching appropriate, peer-reviewed sources, we will summar
recent findings

Study/Article Methods, Findings, Da

Author Abbreviated Title Study Question/Purpose

To review the current literature on

James W. Murrough1, Chadi G. Targeting glutamate signalling in glutamate targeting using
Abdallah2 and Sanjay J. Mathew depression: progress and prospects modulators for the treatment of
depression.

Lorenz Deutschenbaur, Johannes

To provide insights into the efficacy
Beck, Anna Kiyhankhadiv,
Role of calcium, glutamate and of using gluatmate modulators and
Markus Mühlhauser, Stefan
NMDA in major depression and the interactions that occur with
Borgwardt, Marc Walter, Gregor
therapeutic application calcium when drugs like ketamin
Hasler, Daniel Sollberger, Undine
are used for treatment
E. Lang

To present the neurpplasticity

Towards a glutamate hypothesis of
Gerard Sanacora, Giulia Treccani, and Maurizio Popoli hypothesis for mood/anxiety
depression
disorres and the interplay with stress

To test the clincaly efficay of

Mehdi Ghasemi, Cristy Phillips, Mechanisms of action and clinical
NMDA modulators on depression
Atoossa Fahimi, Margaret Windy efficacy of NMDA receptor
and to expand on thte current
McNerney, Ahmad Salehi modulators in mood disorders
challenges for drug development
Wei Zheng, Yan-Ling Zhou, Wei- Neurocognitive performance and
To test the neurocognitive
Jian Liu, Cheng-Yu Wang, Yan-Ni repeated-dose intravenous
effects/depression severity of
Zhan, Han-Qiu Li, Li-Jian Chen, ketamine in major depressive
ketamine infusions
Ming-D Li, Yu-Ping Ning disorder

Study/Article Methods, Findings, Da

Author Abbreviated Title Study Question/Purpose

To present new evidence on the effects

of antidepressants in neuronal
Samuel J. Leistedtn, Paul Brain, networks, depression, connectivity and to describe the
Linkowski and more complexity of brain networks and the
biological mechanisms of depression

To provide evidence such as genetic

modifications of receptors, imaging
studies, mechanisms of plasticity,
Eero Castrén Is mood chemistry? etc. to explain why the network
hypothesis has been adopted by
pharmacologists and
neuropsychologists

Synaptic Mechanisms To explain that ketamine mediates

long-term anti-depressant effects by
Ege T. Kavalali, Ph.D. Lisa M. Underlying Rapid
blocking NMDA receptors resulting
Monteggia, Ph.D. Antidepressant Action of in several processes that contribute
Ketamine to synaptic plasticity

To gather evidence that suggests

Neurotrophic effects of
Eero Castrén
antidepressant drugs
neurogenesis and synaptic
connectivity are induced by
antidepressants, thus improving the
long-term ability for the nervous
system to process information and
elevate mood
 Study/Article Methods, Findings, D

Author Abbreviated Title Study Question/Purpose

Craig A. Stockmeiser, Laura A. Increase in Serotonin-1A Tests the hypothesis
Hypothesis: that serotonin-
Variation in the
Sylvie L., Gustavo T., David
Shapiro, Ginny E. Dilley, Tamara Autorecepotros in the midbrain of 1A receptors are increased in the
sequence of the repressor region
Bakish., Lisheng D., Pavel
N Kolli, Lee Friedman, andH. Impaired
Suicide repression
Victims withatMajor
a 5- dorsal
may lead to impared repressionwith
raphe of suicide victims of
Christopher
Valentina G.,B.,
Grazyna AdolfoO.,
Grainne S.,Sheena
Rajkowska Neena Hydroxytryptamine
Ketamine 1A Receptor
elicits sustained
Depression To5-HT1A
testmajor
the influence of 5-HT
depression.
the receptor and might
K.,
C.,Stephen
DanielleM.,
E.,Ajoy N., G.,
Sinead Xiao O.,
and Gene Polymorphism
antidepressant-like activity via a depletion on the antidepressant-like
correlate with depression or sucidal
and Paul H.
Andrew A. serotonin-dependend mechansim effectbehavior.
of ketamine.

A report highlighting how seratonin

Mechanism of action of seratonin
Sephen S. selective reuptake inhibitors (SSRIs)
selective reuptake inhibitors
function.

Study/Article Methods, Findings, Da

Author Abbreviated Title Study Question/Purpose
To address and show relevant evidence
on how external factors directly
interfere with neurobiological
mechanisms and functions involved in
van den Bosch, M., & Meyer- Environmental Exposure and the development of depression. The
Lindenberg, A. Depression research findings were cross-analyzed
with the social and cultural aspects of
how our living environment may
increase or decrease the risk of
depression.

To determine if physical activity

Physical Activity and the (PA) can prevent future depression
Mammen, G., & Faulkner, G.
Prevention of Depression as well as examine the amount of PA
required to avoid depression.

To collect available evidence and

Social interventions: An effective characterize the types of social
Nagy, E., & Moore, S. approach to reduce adult interventions that have been conducted
depression? to address depression in general adult
populations.

To highlight the public health impact of

major depression and provide
The Public Health Impact of Major
McLaughlin K. A. recommendations for developing
Depression preventive interventions for depression
and possible public health approaches.
 Review of the Literature Grid
Leslie Bruce

e different texts you read to write your review. Return to it later to help you synthesize the texts as you write. **DUE at the time of your c

ed sources, we will summarize and synthesize the latest research on depression treatment. We will write a research review
recent findings in this research area.

Methods, Findings, Data, Facts, Quotations, Figures, etc. from the Article/Study (include page number
Methods & Usefulness Conclusions or Findings

Ketmaine-like drugs also mediate

Post-mortem studes and prelimiany clincal
monoamine signalling, preclincal
trials that require larger sample sizes and
studies show rapid pyschomimetic
better methodology.
effects and sustained BDNF levels.

Glutamate is the key neurotransmitter

involved in longer term neural
Post-mortem studes and prelimiany clincal
curcuity changes (LTP and LTD).
trials that require larger sample sizes and
Curent anti-dperessents are indirectly
better methodology.
influencing gluatmate
(release/uptake).

Glutamate activates NMDA and

AMPA receptors that are key for
Animal models were used, rats, for these elarning and memory. Ketamine
studies. There is an issue of translationality. paried with current anti-dperessants
as well as selective NMDA-R
antagonists have increased efficacy.

NMDAR antagonists produce rapid

Preliminary clinial studies and animal
antipressant effects, reduce
models were used and require better
inflamatorry effects, and aid in
methodology and translationality for robust
synaptogenesis in individuals with
human studies.
major depression
 One of the first human trials to use
Ketamine infusions have effect on
ketamine for major depression treatement.
processing speed and verbal learning
Attrition is a confounding variable

Methods, Findings, Data, Facts, Quotations, Figures, etc. from the Article/Study (include page number

Methods & Usefulness Conclusions or Findings

Anti-depressants activate plasticity

rodent models, fMRI and PET, genetic processes, thus improving
methods information processing involved in
mood regulation

Plasticity of neural connections are

Imaging studies, genetic manipulation of crucial during early development.
neural circuits through in vivo recording Antii-depressants can reorganize
techniques and behavioral assays specific connections that have been
altered.

"the blockade of spontaneous NMDA

A review that mentions animal models, and
molecular and functional studies
receptors and the inhibition of eEF2
kinase to up- regulate dendritic protein
translation [act] as the trigger for
ketamine’s fast-acting antidepressant
action" (pg.4)

An increase in BDNF levels and trkB

Post-mortem studies, animal models
(rodent), brain imaging and
neuropathalogical studies
signaling are necessary for mood
elevation that results from the
administration of anti-depressants.
Anti-depressants may recover some
of the morphological changes that
occur in the brain.
 Methods, Findings, Data, Facts, Quotations, Figures, etc. from the Article/Study (include page number)
This paper provides one of the first
Post-mortem Methods & Usefulness
study quantifying the amount analysis on a genotype
Conclusions affecting and
or Findings
of Seratonin-1A receptors along the dorsal influencing the depression phenotype.
There is significant evidence of
In vitro
raphe. analysis
Using of
suicide single
victimsnucleotide
compared Specifically,
increased it provides
serotonin-1A information
receptors
Thepolymorphisms
role of ketamine was PCR,
using assessed on mice
Electro- that the
a single nucleotide
against to
subjected natural
5-HT death patients
depletion and using a 5- throughout
stress. Highlights midbrain
the ofdorsal
role is 5-HT raphe.
in be
mobility
seratonin-1A shift assays,
binding agentgene reporter
[H]-OH-DPAT. polymorphism (SNP) found to
HT was repressed via a tryptophan
systems, and microscopy. inhibitor sustaining antidepressant
most prevalent within activity of
and physical stress induced by physical ketamine.
depressed/suicide victims.
restraint.
This paper is a review and is useful in that SSRIs functin by binding
Furthermore, to sites
it analyzes how that
it will help us understand how SSRIs help transcription
decrease transporter
is affectedaffinity
by this for
SNP.
treat depression, why SSRIs don't work for serotonin and inhibiting subsequent
everyone, and why SSRIs become serotonin binding. Serotonin
ineffectual over time. accumulates within the synapse.

Methods, Findings, Data, Facts, Quotations, Figures, etc. from the Article/Study (include page number
Methods & Usefulness Conclusions or Findings
Harmful exposures like air pollution,
The research is useful because it provides noise, pesticides, human-made
evidence and example of how different electromagnetic fields (EMFs) can
environmental exposures can affect the increase the risk of depression as well as
function in the brain as well as directly and urbanization, and natural disasters could
indirectly increase the risk of depression. It increase the prevalence of depression. On
will also show how a human's contextual the other hand, exposure to the natural
environment can increase or decrease the environment can reduce the risk of
prevalence of depression. depression and promote healthy
behaviors.

A comprehensive search was conducted from 25 of the 30 studies demonstrated evidence

July 2012 to February 2013 in various databases that PA may prevent future depression (pg.
to analyze the data collected in chosen articles 649). The researchers found promising
to examined the relationships between physical evidence that any level of PA, including low
activity and depression over at least two time levels (e.g., walking<150 minutes/weeks), can
intervals. prevent future depression.

It explains how social determinants such as
social isolation can increase a person's
likelihood to develop depression as well as
impact the spread at a population level.
Social interventions that were found to reduce
depressive symptoms were skill building, peer
support, psycho-education, psychotherapy,
exercise, group-based activities and links to
community resources.

A multilevel approach to the prevention

The research is useful because it shows why
depression is considered to be a prevalent and
disabling condition that constitutes a significant
public health problem in the United States. It also
gives information on the epidemiological aspect of
depression.
of depression must include interventions
targeting individuals, community, and
structural determinants and is necessary
to adequately improve population health
and decrease the growing burden of
depression.
size the texts as you write. **DUE at the time of your conference.

ession treatment. We will write a research review article summarizing

m the Article/Study (include page number)

Remaining Questions or Relation to Review Topic &
Uncertanties Other Articles

There are still uncertainties in the

This article supports the
role glutamate targetting may have
introduction of the neurplasticity
with curent drug treaments and
hypotheis and ketamine's rapid
more generally, diagnosing
efficacy.
treatment-resistant patients

This article reviews the efficacy of

Most of the curentstudes
glutamate modulators in animal
conducted on these drugs has been
models to supprt their use as
done on animlas, human studies
treatment. It corroborates the
are still needed.
findings in Ghasemi et al. (2017).

This article introduces the shift

There are various mechanisms at form a monoamine hypothes to a
play that overlap and may have neuroplsticity hypothesis. It argues
downstream effects when that long term changes in neural
gluatmate is targetted. circutiy may be influenced buy
glutamate.

With the multitude of NMDA This article helps to expand on

modulators, there is still the efficacy of various NMDa
question of how to develop a drug modualtors, like ketamine, and
that can be given to treatment- explains curents challenges for
resistant patients. their use as treatment.
 Dosage amounts have harmful This article aids in discussing the
effects on neurocognition, Further potential use of ketamine to treat
studies are needed. major depression.

m the Article/Study (include page number)

Remaining Questions or Relation to Review Topic &

Uncertanties Other Articles

How can we use a more This is a review that introduces tha

multidisciplinary approach to monoamine theory and then highlights
the network theory as a means for
better understand the heterogeneity researching the affects of anti-
of depression and its symptoms, or depressants on the brain networks of
can we at all? depressed patients.

Which neuronal networks are Much of this paper was used to

involved in the development of write the review by Leistedtn and
depression and are they the same Linkowski (a lot of very similar
in all affected patients? chunks)

This study was based on low doses

of ketamine, do higher doses rely
This article explain's ketamine's
on the same signaling pathways?
rapid efficacy as a result of specific
Also, the ketamine effect is mostly
synaptic mechanims in the
present in the hippocampus, can
hippocampus
other regions in the CNS be
specfied?

This review highlights BDNF

Is anything else activated involvement in the mechanism of
downstream of trkB that is depression. It also discusses the
involved in the behavioral effects mechanism of neurogenesis and
of antidepressants? neuronal turnover as processes that
facilitate neuronal connectivity
m the Article/Study (include page number)

Remaining
Are Questions
the serotonin or
receptors Relation to Review Topic & Other
different Uncertanties
Are more gene/gene they
in any way or are Articles
This paper provides
In relation evidence
to our review, of the
this paper
justpolymorphisms
present in moreinvolved
quantity?inAnd
role seratonin
provides receptors
evidence that play
genes
May help bridge the gap between in
may
why are they present
affecting different typesin of
greater
5-HT
thecause depression.
the depression phenotype.
serotonin/ketamine theories and
amounts for
receptors? depressed/suicide
How can
How effective was the 5-HTthis
victims? Moreover,
how sharedtargeting these
receptors maygenes
be
information
depletion system beused
usedinasmice?
a
may provide
targeted a therapeutic
by different avenue.
treatments (ie
therapeutic target?
SSRIs and Ketamine)
Understanding how SSRIs
Not answered by this paper are
function will help us understand
how other drugs may have an
why this treatment option is
effect on serotonin reuptake.
prevalent today and its limitations.

m the Article/Study (include page number)

Remaining Questions or Relation to Review Topic &
Uncertanties
The primary reason to use some of
the environmental exposures have
many beneficial outcomes
(pesticides & EMFs) so, a careful
trade-off analyses must be
conducted together with increased
international investments in
finding alternative strategies and
protection measures.
Other Articles
The article talks about the different
biological, social, and environmental
exposure that can increase or decrease
the risk or prevalence of depression.
Additionally, it provided examples of
how certain harmful exposure could
affect the function of the central
nervous system and certain
neurotransmitters.

Is there enough evidence to assume

Physical activity can serve as a
that physical activity can treat
valuable mental health promotion
depression thus allowing patients
strategy in reducing the risk of
to avoid physiologic side effects
depression for individuals and the
and costs associated with
population.
prescribed antidepressants?

The various types of social interventions

Will the same results show for
people with chronic depression and
postpartum depression?
that were studies can effectively reduce
adult depression, and it efficiently
implements into different types of
communities including communities with
less available resources.

How do they plan to implement this To develop universal prevention in

multilevel approach in non-middle depression, Public health professionals
class or wealthy communities that need to aid mental health professionals in
have fewer community resources as evaluating the effects of global preventive
well as countries with a prevalence in interventions at a community or population
poverty? level.