Dr. Kratter is a fellowship-trained psychiatrist and clinical assistant professor in the Department of Psychiatry & Behavioral Sciences at Stanford University School of Medicine. He is also director of Invasive Technologies in the Stanford Brain Stimulation Laboratory.
His clinical interests include depression, obsessive-compulsive disorder, eating disorders, sleep disorders, adult autism spectrum disorder, Huntington’s disease, and neuropsychiatric predictors of outcomes following deep brain stimulation for Parkinson’s disease.
His research interests include deep brain stimulation and neuroimaging. He is a co-investigator of a study of deep brain stimulation for obsessive-compulsive disorder. He is also a co-investigator of a study exploring the use of individualized neuroimaging biomarkers to predict OCD patients’ response to repetitive transcranial magnetic stimulation (rTMS). This therapy is a noninvasive form of brain stimulation that uses a magnet to stimulate targeted areas of the brain. Both studies are supported by the Foundation for OCD Research
Dr. Kratter has published articles on topics such as deep brain stimulation for Parkinson’s disease and gene-targeting therapy for Huntington disease. His work has appeared in the Journal of Clinical Investigation, Proceedings of the National Academy of Science, and American Journal of Human Genetics. He also co-authored the chapter on major depression in the textbook Deep Brain Stimulation: Techniques and Practice.
Dr. Kratter has presented his work at the annual meetings of the American Neuropsychiatric Association, Hereditary Disease Foundation, and Society for Neuroscience. Topics include cognitive changes following deep brain stimulation for Parkinson’s disease, antipsychotic-induced thrombocytopenia, and mediators of pathology in Huntington’s disease.
For his scholarship and research achievements, Dr. Kratter has won numerous honors. They include the Miller Foundation Award for Psychiatric Research. He also won the Ruth L. Kirschstein National Research Service Award from the National Institute of Neurological Disorders and Stroke.
He is or has been a member of the American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, American Association for Geriatric Psychiatry, Academy of Psychosomatic Medicine, and Society for Neuroscience.
Clinical Assistant Professor, Psychiatry and Behavioral Sciences
Clinical Assistant Professor, Psychiatry and Behavioral Sciences
Honors & Awards
Molecular and Cell Biology Departmental I.L. Chaikoff Award, UC Berkeley (2005)
Fellowship, Medical Scientist Training Program (MSTP) , UCSF (2006)
Ruth L. Kirschstein National Research Service Award (F31), National Institute of Neurological Disorders and Stroke (NINDS). (2011)
National Residency Team Competitor, American Psychiatric Association MindGames (2017)
Honors Scholar, American Association for Geriatric Psychiatry (AAGP) (2018)
Best Poster Award for a Medical Trainee, University of Pittsburgh Department of Psychiatry Research Day (2019)
Miller Award for Psychiatric Research, Miller Foundation, Stanford University School of Medicine (2020 - 2021)
Board Certification: American Board of Psychiatry and Neurology, Psychiatry (2019)
Fellowship: Stanford University Psychiatry and Behavioral Sciences (2020) CA
Residency: Western Psychiatric Institute and Clinic (2019) PA
Medical Education: University of California San Francisco Registrar Office (2015) CA
Anterior Sensorimotor Subthalamic Nucleus Stimulation Is Associated With Improved Voice Function.
BACKGROUND: Despite the impact of Parkinson disease (PD) on speech communication, there is no consensus regarding the effect of lead location on voice-related outcomes in subthalamic nucleus (STN) deep brain stimulation (DBS).OBJECTIVE: To determine the relationship of stimulation location to changes in cepstral analyses of voice following STN DBS.METHODS: Speech pathology evaluations were obtained from 14 PD subjects, before and after STN DBS, including audio-perceptual voice ratings (overall severity, loudness, hoarseness changes), measured indices of dysphonia (cepstral peak prominence and cepstral spectral index of dysphonia), and phonatory aerodynamics. The contact locations used for active stimulation at the time of postoperative voice evaluations were determined and assessed in relation to voice outcomes.RESULTS: Voice outcomes remained relatively unchanged on average. Stimulation locations in the anterior portion of the sensorimotor region of the left STN, however, were associated with improvements in voice severity scores, cepstral spectral index of dysphonia, shortness of breath, and phonatory airflow during connected speech. Posterior locations were associated with worsening of these outcomes. Variation in the medial-lateral or dorsal-ventral position on the left, and in any direction on the right, did not correlate with any voice outcome.CONCLUSION: Active contact placement within the anterior sensorimotor STN was associated with improved perceptual and acoustic-aerodynamic voice-related outcomes. These findings suggest an STN topography for improving airflow for speech, in turn improving how PD patients' voices sound.
View details for DOI 10.1093/neuros/nyaa024
View details for PubMedID 32199026
- DBS in major depression Deep Brain Stimulation: Techniques and Practice Thieme Medical Publishers. 2019
Serine 421 regulates mutant huntingtin toxicity and clearance in mice
JOURNAL OF CLINICAL INVESTIGATION
2016; 126 (9): 3585–97
Huntington's disease (HD) is a progressive, adult-onset neurodegenerative disease caused by a polyglutamine (polyQ) expansion in the N-terminal region of the protein huntingtin (HTT). There are no cures or disease-modifying therapies for HD. HTT has a highly conserved Akt phosphorylation site at serine 421, and prior work in HD models found that phosphorylation at S421 (S421-P) diminishes the toxicity of mutant HTT (mHTT) fragments in neuronal cultures. However, whether S421-P affects the toxicity of mHTT in vivo remains unknown. In this work, we used murine models to investigate the role of S421-P in HTT-induced neurodegeneration. Specifically, we mutated the human mHTT gene within a BAC to express either an aspartic acid or an alanine at position 421, mimicking tonic phosphorylation (mHTT-S421D mice) or preventing phosphorylation (mHTT-S421A mice), respectively. Mimicking HTT phosphorylation strongly ameliorated mHTT-induced behavioral dysfunction and striatal neurodegeneration, whereas neuronal dysfunction persisted when S421 phosphorylation was blocked. We found that S421 phosphorylation mitigates neurodegeneration by increasing proteasome-dependent turnover of mHTT and reducing the presence of a toxic mHTT conformer. These data indicate that S421 is a potent modifier of mHTT toxicity and offer in vivo validation for S421 as a therapeutic target in HD.
View details for DOI 10.1172/JCI80339
View details for Web of Science ID 000382513400036
View details for PubMedID 27525439
View details for PubMedCentralID PMC5004962
Sequence-Level Analysis of the Major European Huntington Disease Haplotype
AMERICAN JOURNAL OF HUMAN GENETICS
2015; 97 (3): 435–44
Huntington disease (HD) reflects the dominant consequences of a CAG-repeat expansion in HTT. Analysis of common SNP-based haplotypes has revealed that most European HD subjects have distinguishable HTT haplotypes on their normal and disease chromosomes and that ∼50% of the latter share the same major HD haplotype. We reasoned that sequence-level investigation of this founder haplotype could provide significant insights into the history of HD and valuable information for gene-targeting approaches. Consequently, we performed whole-genome sequencing of HD and control subjects from four independent families in whom the major European HD haplotype segregates with the disease. Analysis of the full-sequence-based HTT haplotype indicated that these four families share a common ancestor sufficiently distant to have permitted the accumulation of family-specific variants. Confirmation of new CAG-expansion mutations on this haplotype suggests that unlike most founders of human disease, the common ancestor of HD-affected families with the major haplotype most likely did not have HD. Further, availability of the full sequence data validated the use of SNP imputation to predict the optimal variants for capturing heterozygosity in personalized allele-specific gene-silencing approaches. As few as ten SNPs are capable of revealing heterozygosity in more than 97% of European HD subjects. Extension of allele-specific silencing strategies to the few remaining homozygous individuals is likely to be achievable through additional known SNPs and discovery of private variants by complete sequencing of HTT. These data suggest that the current development of gene-based targeting for HD could be extended to personalized allele-specific approaches in essentially all HD individuals of European ancestry.
View details for DOI 10.1016/j.ajhg.2015.07.017
View details for Web of Science ID 000361084700006
View details for PubMedID 26320893
View details for PubMedCentralID PMC4564985
Targeting H3K4 trimethylation in Huntington disease
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
2013; 110 (32): E3027–E3036
Transcriptional dysregulation is an early feature of Huntington disease (HD). We observed gene-specific changes in histone H3 lysine 4 trimethylation (H3K4me3) at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD.
View details for DOI 10.1073/pnas.1311323110
View details for Web of Science ID 000322771100015
View details for PubMedID 23872847
View details for PubMedCentralID PMC3740882
PolyQ Disease: Too Many Qs, Too Much Function?
2010; 67 (6): 897–99
The nature of the gain-of-function toxicity found in polyglutamine (polyQ) diseases has been the subject of considerable debate. In this issue of Neuron, Duvick et al. and Nedelsky et al. show that, in two of these diseases, pathology is mediated by normal protein activity.
View details for DOI 10.1016/j.neuron.2010.09.012
View details for Web of Science ID 000282801100001
View details for PubMedID 20869586
View details for PubMedCentralID PMC3989162
Stereoselective macrocyclization through zirconocene-mediated coupling of achiral dialkynes
1,4-Bis[trimethylsilyl(ethynyl)]naphthalene () and 1,4-bis[trimethylsilyl(ethynyl)]anthracene () undergo diastereoselective coupling with Cp2Zr(py)(Me3SiC[triple bond, length as m-dash]CSiMe3) to give trimeric macrocycles in good yield.
View details for DOI 10.1039/b815750b
View details for Web of Science ID 000261960400026
View details for PubMedID 19099079