Tag Archives: www.novaketamine.com

703-844-0184 | KETAMINE INFUSIONS |KETAMINE for DEPRESSION | KETAMINE – ENJOY LIFE, DON’T JUST WALK THROUGH LIFE | KETAMINE DOCTORS IN VIRGINIA | FAIRFAX KETAMINE | 703-844-0184 | KETAMINE AND DEPRESSION TREATMENT – Newsweek Article | 22308 |22305 | 22304 | 22191 |22192 |22193 | 20118 | 20104 | KETAMINE TREATMENT FOR DEPRESSION CBS News – Ketamine for Suicidal ideation |CRPS |RSD |KETAMINE INFUSIONS FOR PAIN | SPRINGFIELD , VA KETAMINE |

CAll  nitrous oxide and viagra entrance essay examples go here thesis content page cialis necessita di ricetta medica best way to start a research paper introduction https://www.lapressclub.org/hypothesis/essays-about-novels-samples/29/ thesis argument outline see url here how much does generic synthroid cost out of pocket source site https://thejeffreyfoundation.org/newsletter/essay-writer-review/17/ logics business plan poor thesis statements http://www.danhostel.org/papers/technical-paper-writing-tips/11/ https://cwstat.org/termpaper/essay-about-ethical-leadership/50/ classroom management dissertations essays about childhood development viagra price nigeria achat viagra rapide examples of essay references https://onlineinfo.hartford.edu/dosage/keine-wirkung-mit-viagra/39/ cuhk thesis latex template here essay on why should schools have uniforms https://mysaschool.org/expository/expository-essay-writing-lesson-plan/15/ see url an essay on karma enter site coughlan thesis enter site 703-844-0184 for an immediate appointment!

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

amoxicillin and birth control side effects
High blood pressure and orgasm are incompatible
viagra order
clomid drug dosage conversion
is propecia an effective drug
amoxicillin pregnancy teeth
Hydroxychloroquine Aralen (Chloroquine) malaria price
acquistare viagra orodispersibile pagamento online
viagra ervaringen
generic drug costs without insurance
acquistare Viagra 25 mg online sicuro
buy cialis uk
what should cialis pills cost with perscription
acquistare Viagra 50 mg online
acquistare cialis senza ricetta Roma
effect of propecia
Tadalafil vs Sildenafil
imuran drug category of synthroid
Hydroxychloroquine buy
Aralen (Chloroquine) generic coronavirus price
Ketamine | Fairfax, Virginia | 703-844-0184 | Ketamine infusions for depression | Dr. Sendi | Ketamine for alcoholism and drug abuse Ketamine in Maryland |IV ketamine treatments| NOVA Health Recovery |

Below is the latest on CBS for Ketmine treatment for Depression. Don’t Just walk through life..enjoy it.

Ketamine has been very successful in treating depression and suicidality in many patients over a long period of time:

Image result for suicidal person
703-844-0184 | Ketamine for Depression | Virginia |Fairfax | Loudon | Alexandria Ketamine infusions | PTSD | Anxiety

Ketamine gaining popularity as a treatment for the severely depressed

amoxicillin rash scars
Men after 60 are not interested in sex
viagra prescription cost
new fertility drug like clomid twins
fin car vs proscar drug
amoxicillin dosage pneumonia
Aralen (Chloroquine) generic buy
edinburgh articleid charles linskaill viagra
sal tropine generic drug
acquistare viagra generico 100 mg consegna rapida a Milano
best price for cialis
chemical name of cialis
acquistare Viagra in farmacia senza ricetta
acquistare tadalafil senza ricetta Lazio
propecia discussion
is there any generic drug for viagra
synthroid doses drugs
Hydroxychloroquine Plaquenil generic coronavirus
Aralen (Chloroquine) generic drug price
Anne Stallings says she has been battling severe depression for most of her life. She tried anti-depressants and even electroconvulsive therapy, but nothing worked until she went to a Ketamine  clinic  and tried ketamine, reports CBS News correspondent Paula Reid. 
 
“It was like the fifth treatment in and I had come home from the grocery store and I was putting away the groceries and I was like, ‘Wow, this is how you don’t feel depressed.’ It was like from turning on a black and white TV to a color TV,” Stallings said.   
 
Ketamine was approved by the FDA in the 1970s to sedate patients during medical procedures. It is more commonly known as an animal tranquilizer and in powder form as “Special K,” a club drug used to get high.
 
Today, ketamine is being provided legally off-label to treat depression at an estimated 250 clinics across the U.S.

ctm-saturday-clean-feed-20180203-cr470c-0700-0900-01-frame-72699.jpg

Anne Stallings

 CBS NEWS

amoxicillin 500 mg missed dose
Can a man understand when it’s time to worry about impotence
Clomid ovulation symptoms
buy finpecia 1mg uk online
generic viagra discount cheap
Aralen (Chloroquine) malaria coronavirus
miglior sito per acquistare viagra generico 50 mg a Napoli
buy cialis next day delivery
cialis jelly black
compro viagra a Verona
is proscar 5mg available in generic
synthroid weight loss
Hydroxychloroquine generic buy
Dr. Steve Levine offers intravenous ketamine infusions at several clinics around the country as an alternative to common anti-depressants. He says he treats about 70-80 patients across all the offices on any given day.

canadian healthcare female viagra
acquistare brand Viagra
Plaquenil generic virus protection
“Everything for the past 50 years has been based on the chemical imbalance theory of depression which has never held water,” Levine said. “So all these medicines, while they do help a lot of people, are based upon a flawed theory. And that is probably one of the reasons why they do take so long to work. They all take weeks to months to work so here is a medicine that people can take infrequently that is based upon a theory of the brain that makes a lot more sense and it works almost immediately.”
 
Stallings didn’t have time to wait. She had an especially hard time over the holidays and when her father got sick, she thought about taking her own life.
 
“I actually had suicidal ideations and the one thing about ketamine was that I was able to get in here emergently because I knew what was going on and when I left here my suicidal thoughts were gone,” Stallings said. 
 
That is in line with what Columbia University discovered in one of the largest studies yet on ketamine. Researchers found the drug was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients. The effects lasted up to six weeks.
 
Twenty-two-year-old Marc Nelson ditched his antidepressants for ketamine and talk therapy. He says he now feels more like himself, but it came at a cost. He has spent more than $10,000 on treatments.
 
“So many different drugs that I am now off of all of them, which you know, the side effects were just not tolerable to me. They make me a zombie. I was not happy,” Nelson said. 
 
But these infusions can have their own pitfalls. Ketamine can cause people to feel detached from their bodies.

ctm-saturday-clean-feed-20180203-cr470c-0700-0900-01-frame-74486.jpg

Marc Nelson receives a ketamine treatment 

 CBS NEWS

“The 45-minute period of very floatiness, I sometimes get nauseous,” Nelson said. “It’s a very interesting process. … I just lost my train of thought.”
 
Once the treatment was finished, Nelson said he felt “clear, cognizant” and “definitely able to pronounce” his words again.
 
Asked to address critics who say he’s making money by giving people the opportunity to get high, Levine said, “I would say that if you ask any of our patients none of them feel that they are getting high.”

“People tend to focus on the party use of ketamine, because it is more exciting, it’s sexier in some way. It does it a disservice because that’s a very small fraction of its use,” Levine added. “And as far as the money making aspect of this, if you were doing things in the right way you’re not gonna make a lot of money.”

Ketamine has piqued the interest of some major pharmaceutical companies. There are half a dozen drugs in development that mimic the way ketamine works, with some undergoing FDA clinical trials for approval as antidepressants.

For decades, Dr. Gerry Sanacora has been studying ketamine at Yale.

“What we’re trying to understand is what does it change in the brain that allows that sustained anti-depressant like response?” Sanacora said. 
 
He says the drug is not addictive in the way opioids are, but could still be harmful in the long run.
 
“There is at least evidence in animal models that these type of medications can actually cause some structural damage in the brain. That’s usually at higher doses, that’s usually at longer term exposure but we don’t know where that level is,” Sanacora said. 
 
Dr. Levine said he monitors patients closely. 

“In our population even people who have been having ketamine on a maintenance basis for up to six years now we haven’t seen any sign of that,” Levine said.

But for Anne Stallings, despite the unknowns, she’s content with a chance to feel normal.
 
“If I can live a quality, happy life, and be productive, be able to go to work, to be able to have my family, to enjoy life – not walk through life but enjoy life – then it’s worth it.”

Ketamine for rapid reduction of suicidal thoughts 2017  <article out of Colombia University

In major depression with clinically significant suicidal ideation,
a single subanesthetic ketamine infusion, adjunctive to ongoing
pharmacotherapy, was associated with a greater reduction
in suicidal thoughts at day 1, the primary outcome measure,
compared with midazolam control infusion. The adjusted
mean difference of 4.96 points on the clinician-rated SSI, a
Cohen’s d of 0.75, and a number needed to treat of 4 for
response represent a medium-sized effect. Adverse effects—
mainly blood pressure increase and dissociative symptoms—
were similar to those reported in other ketamine studies (37)
and were mostly mild to moderate, and transient, typically
resolving within minutes to hours after infusion. Improvement
in suicidal ideation largely persisted during the 6-week period of uncontrolled observation, during which
standard pharmacological treatments were also optimized.
To our knowledge, there is no established definition of a
clinically meaningful reduction in score on a standard suicidal
ideation scale. A prospective study (N=6,891) of patients
with depressive disorders (23) found that a baseline SSI
score .2 predicted suicide during up to 20 years of follow-up.
In a prospective study of 562 inpatients (64% with a mood
disorder) who endorsed suicidal thoughts (38), those who
experienced a 50% reduction within 24 hours from a severe
level (suicidal ideation “most of the time”) had one-third the
risk of subsequent self-harm events during a mean length of
stay of 24 days, compared with those whose suicidal thoughts
remained elevated. Given concerns about ketamine’s 1- to 2-week antidepressant
effect in previous studies (11), it is notable that the
improvement in suicidal ideation in this trial was largely
maintained through the 6-week follow-up ratings. This may
be partly explained by the fact that patients continued prior
psychotropic medication, which was optimized after completion
of day 1 postinfusion ratings. Our result is consistent
with the Hu et al. trial (41), in which patients with major depression
who were randomly assigned to receive a single
ketamineinfusion onday 1 of escitalopram therapy experienced
a faster response compared with patients who received a saline
control infusion, and the benefits were maintained for 4 weeks.

We found greater reductions in overall mood disturbance,
depression, and fatigue, assessed with the POMS, on day 1 after
ketamine compared with midazolam.A
secondary analysis of adjunctive ketamine (N=14) found
a reduction in suicidal ideation even when depression did
not remit (17)Ketamine is mechanistically distinct from
currently approved antidepressants, its therapeutic effects
possiblyinvolving rapid synapse formation (44)

Montgomery-Asberg Depression Rating Scale

In summary, in this randomized trial in suicidal depressed
patients, a single adjunctive subanesthetic ketamine infusion
was associated with a clinically significant reduction
in suicidal ideation at day 1 that was greater than with the
midazolam control infusion. In the context of standard, optimized
treatment after the ketamine infusion, this improvement
appeared to persist for at least 6 weeks. The
clinical applicability of our findings was improved with infusion
administration by a psychiatrist and without a medication
washout, as has been done in some studies

Profile of mood states

_Modified_Scale_for_Suicidal_Ideation

KETAMINE INFUSIONS |KETAMINE DEPRESSION | KETAMINE DOCTORS IN VIRGINIA | FAIRFAX KETAMINE | 703-844-0184 | KETAMINE AND DEPRESSION TREATMENT – Newsweek Article | 22308 |22305 | 22304 | 22191 |22192 |22193 | 20118 | 20104 | KETAMINE TREATMENT FOR DEPRESSION |CRPS |RSD |KETAMINE INFUSIONS FOR PAIN | SPRINGFIELD , VA KETAMINE |

NOVA Health Recovery  <<< Ketamine infusion center in Alexandria, Virginia 703-844-0184  – consider ketamine for addiction treatment

CAll 703-844-0184 for an immediate appointment!

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

I sifted through the article and took out several points in the discussion of the article below.:

By taking the focus off “oneself” and placing it on other stimuli,
it is possible that ketamine decreases awareness of negative
experiences and consequently improves mood.

The transient dissociation experienced by depressed patients
during a ketamine infusion may have the effect of dampening
what the hyperactive self-monitoring associated with
depressive illness.

Radiology findings may reflect ketamine’s ability to reclaim frontal control over deeper limbic structures, thus strengthening the cognitive control of emotions and decreasing depressive symptoms.

Ketamine may cause a “disconnect”
in several circuits related to affective processing, perhaps
by shifting focus of attention away from the internal
states of anxiety, depression, and somatization, and more toward
the perceptual changes (e.g., hallucinations, visual distortions,
derealization) induced by ketamine. Similarly,
during an emotion task, ketamine attenuated responses to
negative pictures, suggesting that the processing of negative
information is specifically altered in response to ketamine.57
By taking the focus off “oneself” and placing it on other stimuli,
it is possible that ketamine decreases awareness of negative
experiences and consequently improves mood

Ketamine-Associated Brain Changes A Review of the Neuroimaging Literature

Abstract
Major depressive disorder (MDD) is one of the most prevalent conditions in psychiatry. Patients who do not respond to traditional monoaminergic antidepressant treatments have an especially difficult-to-treat type of MDD termed treatment-resistant depression. Subanesthetic doses of ketamine-a glutamatergic modulator-have shown great promise for rapidly treating patients with the most severe forms of depression. As such, ketamine represents a promising probe for understanding the pathophysiology of depression and treatment response. Through neuroimaging, ketamine’s mechanism may be elucidated in humans. Here, we review 47 articles of ketamine’s effects as revealed by neuroimaging studies. Some important brain areas emerge, especially the subgenual anterior cingulate cortex.

Ketamine-Associated Brain Changes: A Review of the…. Available from: https://www.researchgate.net/publication/323324257_Ketamine-Associated_Brain_Changes_A_Review_of_the_Neuroimaging_Literature [accessed Mar 31 2018].

 

Newsweek article showing that ketamine can help in Depression – 2018

This is the article in Newsweek below:

Ketamine could offer a fast and effective treatment for people with depression, even those who have failed to respond to current therapy options. A new medical reviewpublished this month adds to the growing evidence that the drug could be used in a clinical setting.

The review, published in the Harvard Review of Psychiatry, analyzed 47 studies on ketamine as a treatment for depression. The paper outlined specific ways in which ketamine affected the brains of depression patients.

Ketamine is a drug that can relieve pain and cause feelings of relaxation. It is generally used as an anesthetic in medical setting, but it is also abused as a party drug. Recreational users typically seek a sensation described as being similar to an out-of-body experience. 

A New Drug for Depression

03_05_ketamineKetamine could double as a depression treatment.

Despite its popularity at parties, ketamine has been the subject of numerous clinical studies for its potential to treat depression. Data have been mounting in its favor, and now a team at Harvard Medical School has reviewed the evidence thus far. 

The authors found that many patients given ketamine displayed measurable positive changes in brain activity in areas associated with the ability to process and control emotions, Business Insider reported.

Those changes include activation of the subgenual anterior cingulate cortex—connected to both emotions and cognition—as observed by neuroimaging. The activation was directly associated with improvement of depression symptoms in as little as 24 hours after patients received a single intravenous subanesthetic ketamine dose.

The drug also enhanced how the brain responded to positive emotions, a change indicated by increased connectivity in the right-hemisphere caudate. That enhancement helped relieve symptoms of depression, possibly because of this region’s connection to the brain’s reward system. 

Related: Perfectionists Are More Likely to Be Depressed—But One Thing Might Help Them

Ketamine also appears to decrease the ability to self-monitor, the report noted. This decrease may cause “emotional blunting,” which could help increase reward processing—and, in turn, happiness.

How Does Ketamine Work? 

Although the review did not describe exactly how ketamine produces its antidepressant effect, the authors noted that the effect may be indirect. Past research found that ketamine affects several receptors in the brain, such as opioid receptors, adrenegic receptors and serotinin receptors. The review concluded that the side effects of ketamine’s effect on those receptors may be the root cause of its antidepressant response. However, more research is needed to confirm this. 

Related: Are Nice People More Likely to Be Depressed?

The recent review is the latest scientific publication to suggest that this commonly used (and abused) drug could be an extremely helpful depression treatment.

KETAMINE | FAIRFAX | ALEXANDRIA | 703-844-0184| KETAMINE THERAPY | KETAMINE AS AN ANTI-DEPRESSANT – NIH -| Dr. Sendi | Ketamine Springfield, Va | Ketamine Loudon | Ketamine for depression | email@novahealthrecovery.com

NOVA Health Recovery  <<< Ketamine infusion center in Alexandria, Virginia 703-844-0184  – consider ketamine for addiction treatment

CAll 703-844-0184 for an immediate appointment!

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

 

 

Here is an interesting piece regarding the rapid effects of Ketamine on reversing depression, in specific, making events more pleasurable through modulating the action of Glutamate in the brain.

This article was written by Dr. Zarate:

Ketamine and depression – NIH

Highlight: Ketamine: A New (and Faster) Path to Treating Depression

Two charts show the effect of ketamine or placebo on the Hamilton Depression Rating Scale.

Left: Change in the 21-item Hamilton Depression Rating Scale (HDRS) following ketamine or placebo treatment.
Right: Proportion of responders showing a 50 percent improvement on the HDRS following ketamine or placebo treatment.34

Source: Carlos Zarate, M.D., Experimental Therapeutics and Pathophysiology Branch, NIMH

The most commonly used antidepressants are largely variations on a theme; they increase the supply within synapses of a class of neurotransmitters believed to play a role in depression. While these drugs relieve depression for some, there is a weeks-long delay before they take effect, and some people with “treatment-resistant” depression do not respond at all.

The delay in effectiveness has suggested to scientists that the medication-induced changes in neurotransmitters are several steps away from processes more central to the root cause of depression. One possibility for a more proximal mechanism is glutamate, the primary excitatory, or activating, neurotransmitter in the brain. Preliminary studies suggested that inhibitors of glutamate could have antidepressant-like effects, and in a seminal clinical trial, the drug ketamine—which dampens glutamate signaling—lifted depression in as little as 2 hours in people with treatment-resistant depression.34

The discovery of rapidly acting antidepressants has transformed our expectations—we now look for treatments that will work in 6 hours rather than 6 weeks. But ketamine has some disadvantages; it has to be administered intravenously, the effects are transient, and it has side effects that require careful monitoring. However, results from clinical studies have confirmed the potential of the glutamate pathway as a target for the development of new antidepressants. Continuing research with ketamine has provided information on biomarkers that could be used to predict who will respond to treatment.35Clinical studies are also testing analogs of ketamine in an effort to develop glutamate inhibitors without ketamine’s side effects that can then be used in the clinic.36 Ketamine may also have potential for treating other mental illnesses; for example, a preliminary clinical trial reported that ketamine reduced the severity of symptoms in patients with PTSD. 37 Investigation of the role of glutamate signaling in other illnesses may provide the impetus to develop novel therapies based on this pathway.

One of the imperatives of clinical research going forward will be to demonstrate whether the ability of a compound to interact with a specific brain target is related to some measurable change in brain or behavioral activity that, in turn, can be associated with relief of symptoms. In a study of ketamine’s effects in patients in the depressive phase of bipolar disorder, ketamine restored pleasure-seeking behavior independent from and ahead of its other antidepressant effects. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom—loss of interest in pleasurable activities—which lasted up to 14 days.38 Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. This approach is consistent with the NIMH’s RDoC project, which calls for the study of functions—such as the ability to seek out and experience rewards—and their related brain systems that may identify subgroups of patients with common underlying dysfunctions that cut across traditional diagnostic categories.

The ketamine story shows that in some instances, a strong and repeatable clinical outcome stemming from a hypothesis about a specific molecular target (e.g., a glutamate receptor) can open up new arenas for basic research to explain the mechanisms of treatment response; basic studies can, in turn, provide data leading to improved treatments directed at that mechanism. A continuing focus on specific mechanisms will not only provide information on the potential of test compounds as depression medications, but will also help us understand which targets in the brain are worth aiming at in the quest for new therapies.

PET scan data superimposed on anatomical MRI

PET scans revealed that ketamine rapidly restored bipolar depressed patients’ ability to anticipate pleasurable experiences by boosting activity in the dorsal anterior cingulate cortex (yellow) and related circuitry. Picture shows PET scan data superimposed on anatomical MRI.38

References

1 Analysis based on: US Burden of Disease Collaborators. (2013). The state of US health, 1990–2010: Burden of diseases, injuries, and risk factors.JAMA, 310(6), 591–608. (PubMed ID: 23842577)

2 Walker E. R., McGee R. E., & Druss B. G. (2015). Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis.JAMA Psychiatry72(4), 334-341. (PubMed ID: 25671328)

3 Centers for Disease Control and Prevention (CDC). (2013). Web-based Injury Statistics Query and Reporting System(WISQARSTM). Atlanta, GA: National Center for Injury Prevention and Control, CDC.

4 Insel, T. R. (2008). Assessing the economic cost of serious mental illness.American Journal of Psychiatry, 165(6), 663–665. (PubMed ID: 18519528)

5 Soni, A. (2009). The five most costly conditions, 1996 and 2006: Estimates for the US civilian noninstitutionalized population (Statistical Brief# 248). Rockville, MD: Agency for Healthcare Research and Quality.

6 Murray, F. E. (2012). Evaluating the role of science philanthropy in American research universities (Working Paper No. 18146). Cambridge, MA: National Bureau of Economic Research.

7 Terry, S. F. & Terry, P. F. (2011). Power to the people: Participant ownership of clinical trial dataScience Translational Medicine3(69), 69cm3. (PubMed ID: 21307299)

8 Calculated from: McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortalityEpidemiologic Reviews30(1), 67–76. (PubMed ID: 18480098)

9 Addington, J., Heinssen, R. K., Robinson, D. G., Schooler, N. R., Marcy, P., Brunette, M. F., … & Kane, J. M. (2015). Duration of untreated psychosis in community treatment settings in the United StatesPsychiatric Services: A Journal of the American Psychiatry Association. [Epub ahead of print] (PubMed ID: 25588418)

10 Marshall, M., Lewis, S., Lockwood, A., Drake, R., Jones, P., & Croudace, T. (2005). Association between duration of untreated psychosis and outcome in cohorts of first-episode patients: A systematic reviewArchives of General Psychiatry62(9), 975–983. (PubMed ID: 16143729)

11 Clementz, B., Sweeney, J., Hamm J., Ivleva, E., Ethridge, L., Pearlson, G., … & Tamminga C. (2016). Identification of distinct psychosis biotypes using brain-based biomarkers.American Journal of Psychiatry. (PubMed ID: 26651391)

12 Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox, N. A., Leibenluft, E., … & Pine, D. S. (2010). Attention bias modification treatment: A meta-analysis toward the establishment of novel treatment for anxiety.Biological Psychiatry68(11), 982–990. (PubMed ID: 20887977)

13 Britton, J. C., Bar‐Haim, Y., Carver, F. W., Holroyd, T., Norcross, M. A., Detloff, A., … & Pine, D. S. (2012). Isolating neural components of threat bias in pediatric anxiety.Journal of Child Psychology and Psychiatry53(6), 678–686. (PubMed ID: 22136196)

14 Lent, R., Azevedo, F. A., Andrade‐Moraes, C. H., & Pinto, A. V. (2012). How many neurons do you have? Some dogmas of quantitative neuroscience under revisionEuropean Journal of Neuroscience, 35(1), 1–9. (PubMed ID: 22151227)

15 Zhang, Y., Pak, C., Han, Y., Ahlenius, H., Zhang, Z., Chanda, S., … & Südhof, T. C. (2013). Rapid single-step induction of functional neurons from human pluripotent stem cellsNeuron78(5), 785–798. (PubMed ID: 23764284)

16 Krey, J. F., Paşca, S. P., Shcheglovitov, A., Yazawa, M., Schwemberger, R., Rasmusson, R., & Dolmetsch, R. E. (2013). Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neuronsNature Neuroscience16(2), 201–209. (PubMed ID: 23313911)

17 Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium. (2011). Genome-wide association study identifies five new schizophrenia lociNature Genetics43(10), 969–976. (PubMed ID: 21926974)

18 Schizophrenia Working Group of the Psychiatric Genomics Consortium. (2014). Biological insights from 108 schizophrenia-associated genetic lociNature511(7510), 421–427. (PubMed ID: 25056061)

19 Nishimasu, H., Ran, F.A., Hsu, P. D., Konermann, S., Shehata, S. I., Dohmae, N., … & Nureki, O. (2014). Crystal structure of Cas9 in complex with guide RNA and target DNACell156(5), 935–949. (PubMed ID: 24529477)

20 Chung, K., Wallace, J., Kim, S. Y., Kalyanasundaram, S., Andalman, A. S., Davidson, T. J., … & Deisseroth, K. (2013). Structural and molecular interrogation of intact biological systemsNature497(7449), 332–337. (PubMed ID: 23575631)

21 Colantuoni, C., Lipska, B. K., Ye, T., Hyde, T. M., Tao, R., Leek, J. T., … & Kleinman, J. E. (2011). Temporal dynamics and genetic control of transcription in the human prefrontal cortexNature, 478(7370), 519–523. (PubMed ID: 22031444)

22 Kang, H. J., Kawasawa, Y. I., Cheng, F., Zhu, Y., Xu, X., Li, M., … & Šestan, N. (2011). Spatio-temporal transcriptome of the human brainNature, 478(7370), 483–489. (PubMed ID: 22031440)

23 Li, G., Wang, L., Shi, F., Lyall, A. E., Lin, W., Gilmore, J. H., & Shen, D. (2014). Mapping longitudinal development of local cortical gyrification in infants from birth to 2 years of ageThe Journal of Neuroscience34(12), 4228–4238. (PubMed ID: 24647943)

24 Hill, J., Inder, T., Neil, J., Dierker, D., Harwell, J., & Van Essen, D. (2010). Similar patterns of cortical expansion during human development and evolutionProceedings of the National Academy of Sciences107(29), 13135–13140. (PubMed ID: 20624964)

25 Hawrylycz, M. J., Lein, E. S., Guillozet-Bongaarts, A. L., Shen, E. H., Ng, L., Miller, J. A., … & Jones, A.R. (2012). An anatomically comprehensive atlas of the adult human brain transcriptomeNature,489(7416), 391–399. (PubMed ID: 22996553)

26 Miller, J. A., Ding, S. L., Sunkin, S. M., Smith, K. A., Ng, L., Szafer, A., … & Lein, E.S. (2014). Transcriptional landscape of the prenatal human brainNature508(7495), 199–206. (PubMed ID: 24695229)

27 Willsey, A. J., Sanders, S. J., Li, M., Dong, S., Tebbenkamp, A. T., Muhle, R. A., … & State, M. W. (2013). Coexpression networks implicate human midfetal deep cortical projection neurons in the pathogenesis of autismCell155(5), 997–1007. (PubMed ID: 24267886)

28 Gulsuner, S., Walsh, T., Watts, A. C., Lee, M. K., Thornton, A. M., Casadei, S., … & McClellan, J. M. (2013). Spatial and temporal mapping of de novo mutations in schizophrenia to a fetal prefrontal cortical networkCell154(3), 518–529. (PubMed ID: 23911319)

29 Whiteford, H. A., Degenhardt, L., Rehm, J., Baxter, A. J., Ferrari, A. J., Erskine, H. E., … & Vos, T. (2013). Global burden of disease attributable to mental and substance use disorders: Findings from the Global Burden of Disease Study 2010Lancet382(9904), 1575–1586. (PubMed ID: 23993280)

30 Insel, T. R. (2012). Next-generation treatments for mental disordersScience Translational Medicine4(155), 155ps19. (PubMed ID: 23052292)

31 Hyman, S. E. (2012). Revolution stalledScience Translational Medicine4(155), 155cm11. (PubMed ID: 23052291)

32 Biomarkers Definitions Working Group (2001). Biomarkers and surrogate endpoints: Preferred definitions and conceptual frameworkClinical Pharmacology and Therapeutics, 69(3), 89–95. (PubMed ID: 11240971)

33 McGrath, C. L., Kelley, M. E., Holtzheimer, P. E., Dunlop, B. W., Craighead, W. E., Franco, A. R., … & Mayberg, H. S. (2013). Toward a neuroimaging treatment selection biomarker for major depressive disorderJAMA Psychiatry70(8), 821–829. (PubMed ID: 23760393)

34 Zarate Jr, C. A., Singh, J. B., Carlson, P. J., Brutsche, N. E., Ameli, R., Luckenbaugh, D. A., … & Manji, H. K. (2006). A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depressionArchives of General Psychiatry63(8), 856–864. (PubMed ID: 16894061)

35 Cornwell, B. R., Salvadore, G., Furey, M., Marquardt, C. A., Brutsche, N. E., Grillon, C., & Zarate Jr, C. A. (2012). Synaptic potentiation is critical for rapid antidepressant response to ketamine in treatment-resistant major depressionBiological Psychiatry72(7), 555–561. (PubMed ID: 22521148)

36 Zarate Jr, C. A., Mathews, D., Ibrahim, L., Chaves, J. F., Marquardt, C., Ukoh, I., … & Luckenbaugh, D. A. (2013). A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depressionBiological Psychiatry,74(4), 257–264. (PubMed ID: 23206319)

37 Feder, A., Parides, M. K., Murrough, J. W., Perez, A. M., Morgan, J. E., Saxena, S., … & Charney, D. S. (2014). Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder: A randomized clinical trialJAMA Psychiatry, 71(6), 681-688. (PubMed ID: 24740528)

38 Lally N., Nugent A. C., Luckenbaugh D. A., Ameli R., Roiser J. P., & Zarate C. A. (2014). Anti-anhedonic effect of ketamine and its neural correlates in treatment-resistant bipolar depression.Translational Psychiatry. [E-pub ahead of print] (PubMed ID: 25313512)

39 Smith, M., Saunders, R., Stuckhardt, L., & McGinnis, J. M. (Eds.). (2013). Best care at lower cost: The path to continuously learning health care in America. Washington, DC: National Academies Press. (PubMed ID: 24901184)

40 Chambers, D.A., Glasgow, R.E., & Stange, K.C. (2013). The dynamic sustainability framework: Addressing the paradox of sustainment amid ongoing change.Implementation Science, 8(1), 117. (PubMed ID: 24088228)

41 Ben-Zeev, D., Schueller, S. M., Begale, M., Duffecy, J., Kane, J. M., & Mohr, D. C. (2015). Strategies for mHealth research: Lessons from 3 mobile intervention studiesAdministration and Policy in Mental Health and Mental Health Services Research, 42(2), 157-167. (PubMed ID: 24824311)

42 Mohr, D. C., Burns, M. N., Schueller, S. M., Clarke, G., & Klinkman, M. (2013). Behavioral intervention technologies: Evidence review and recommendations for future research in mental healthGeneral Hospital Psychiatry,35(4), 332–338. (PubMed ID: 23664503)

43 Aitken, M., & Gauntlett, C. (2013). Patient apps for improved healthcare from novelty to mainstream.Parsippany, NJ: IMS Institute for Healthcare Informatics.

https://www.nimh.nih.gov/about/strategic-planning-reports/highlights/index.shtml


I also threw in a reprint of the article from NIH regarding strategic principle #2 to find biomarkers of mental health disorders:

Highlight: GPS for the Brain? BrainSpan Atlas Offers Clues to Mental Illnesses

Image from BrainSpan Atlas shows the location and expression level of the gene TGIF1 in a brain from 21 weeks postconception.

The recently created BrainSpan Atlas of the Developing Human Brain incorporates gene activity or expression (left) along with anatomical reference atlases (right) and neuroimaging data (not shown) of the mid-gestational human brain. In this figure, the location and expression level of the gene TGIF1 is shown in a brain from 21 weeks postconception.

Source: Allen Institute for Brain Science

Technologies have come a long way in mapping the trajectory of mental illnesses. Early efforts provided information on anatomical changes that occur over the course of development. In a step that has been hailed as providing a “GPS for the brain,” the BrainSpan Atlas of the Developing Brain, a partnership among the Allen Institute for Brain Science, Yale University, the University of Southern California, and NIMH—has created a comprehensive 3-D brain blueprint.25 The Atlas details not only the anatomy of the brain’s underlying structures, but also exactly where and when particular genes are turned on and off during mid-pregnancy—a time during fetal brain development when slight variations can have significant long-term consequences, including heightened risk for autism or schizophrenia.26 Knowledge of the location and time when a particular gene is turned on can help us understand how genes are disrupted in mental illnesses, providing important clues to future treatment targets and early interventions. The Atlas resources are freely available to the public on the Allen Brain Atlas data portal. Already, the BrainSpan Atlas has been used to identify genetic networks relevant to autism and schizophrenia.27,28 In both of these studies, the fetal pattern of gene expression revealed relationships that could not be detected by studying gene expression in the adult brain. As most mental illnesses are neurodevelopmental, mapping where and when genes are expressed in the brain provides a fundamental atlas for charting risk.

Brain Atlas NIH