Harvard Catalyst Profiles

Contact, publication, and social network information about Harvard faculty and fellows.

Charles A. Nelson III, Ph.D.

Other Positions

Infant Screening Project[login at prompt]
Available: 07/15/11, Expires: 12/31/22

The goal of this project is to use a variety of neuroimaging, behavioral and genetic assays to identify infants at high risk for developing autism - ideally within the first 6 months of life. Several populations of infants are targeted, including those with a family history of the disorder as well as those with known single gene variants. Following training in our neuroimaging methods, the student will assist lab staff and students in scheduling and testing study participants; will be involved in data processing and data analysis; depending on how much time the student has, may be involved in manuscript preparation.

Available: 05/03/17, Expires: 04/30/22

An important function of the brain is to scan incoming sensory information for the presence of biologically relevant features and process and act on this information. For humans, the most salient signals of emotion are often social in nature, such as expressions of fear or anger. The goal of the current competing renewal is to study the nature and neural architecture of emotion processing across the first three years of life. Five-, seven-, and twelve-month-old infants, as well as three-year-old typically developing children will serve as participants across 5 specific aims. Aim 1 seeks to examine the neural correlates of the infant's ability to process emotion in both faces and non-face stimuli. Aim 2 examines a similar question, except that autonomic activity (skin conductance and pupil diameter) will be recorded in conjunction with functional Near Infrared Spectroscopy (fNIRS). Aim 3 seeks to elucidate the neural networks involved in emotion processing, and will do so by using state-of-the-art signal processing software to extract theta activity from the ongoing EEG. Aim 4 will focus on individual differences in emotion processing viewed through the lens of genetics; specifically, all infants serving as participants in Aims 1 and 2 will be genotyped, with most attention focused on 5 single-nucleotide polymorphisms (SNPs), with an additional 5 SNPs serving as a secondary aim. All SNPs have been shown to be relevant to emotion processing in both humans and non-human species. Finally, in Aim 5 we examine whether early biases in emotion processing (i.e., whether infants show greater visual or neural activity to one emotion vs. another; e.g., fear) predict (or are associated with) behavioral inhibition and anxiety. Although the current project focuses on typically developing children, this work has enormous implications for children and adults who suffer from deficits in social-emotional communication. First, this work seeks to explicate the ontogeny of facial emotion processing, an ability that likely provides a foundation upon which higher-level social communication builds. As a result, it may well be the case that errors in this ability that occur early in development can develop into more insidious deficits that occur later in development. Second, the approach adopted in this project is highly innovative, and can easily be extended to various clinical populations, such as toddlers with autism or children diagnosed with depression or bipolar illness. Areas of potential involvement for medical students: • They could participate in data collection or other existing part of the study • They could use the data to address a new research question

Available: 07/01/17, Expires: 03/31/22

The proposed project will rigorously test an evidence-based intervention that is developmentally-informed, child centered, and focused on early social-communication deficits of joint attention and joint engagement. Given the paucity of data on the effectiveness of behavioral intervention for infants with TSC and the lack of biomarkers of treatment response for ASD more generally, our primary goal is to determine if behavioral indices of social communication function can be improved with a targeted, short terms intervention, if these improvements endure 12 months after intervention, and whether this change is reflected in, and can be predicted by, electrophysiological indices of neural processing. We will accomplish this goal by comparing behavioral and EEG outcomes in the treatment group with the outcomes of those on the wait list, while they receive “care as usual” in the community, which can include behavioral intervention. Then after the randomized controlled trial, in a cross sectional analysis, we will compare social communication skills in the entire group of children who received intervention (60 children, 30 at UCLA, 30 at BCH) (twelve months after the end of intervention) with an age matched cohort of children with TSC who have never received treatment (42 children, 21 at UCLA, 21 at BCH) either due to age, distance from testing sites, or other factors that may have precluded their enrollment in the treatment trial. There will be variability in epilepsy and tuber burden, and we will try to understand their effect on treatment response. The only epilepsy-based exclusionary criterion is epilepsy surgery during the study period as surgery may undermine the family’s ability to participate in the treatment process. Areas of potential involvement for medical students: • They could participate in data collection or other existing part of the study • They could use the data to address a new research question

Available: 11/26/19, Expires: 08/31/21

The goal of this pilot project is to identify whether neurotypical individuals display a form of plasticity/learning that has been robustly documented in the mouse and may have potential as a biomarker of neurogenetic and neurodevelopmental disorders. Of highly penetrant genetic contributors to autism spectrum disorders (ASD), intellectual disability (ID) and language delay, copy number variations of the human 16p11.2 region are leading causes (1, 2). The 16p11.2 deletion has been reported to occur in up to 1% of patients with ASD (3-5). Much work is still required to identify biomarkers for patient stratification and therapeutic assessment. Studies in Charles Nelson's lab using human subjects with the chr16p11.2 deletion have revealed increased visual evoked potential (VEP) amplitude over occipital cortex compared to neurotypical, age-matched individuals. Mark Bear's lab at MIT has also identified alterations in visual cortical physiology in the mouse model of human chr16p11.2 micro-deletion (6) that lead to augmented VEP amplitude. Not only did Mark Bear's lab observe elevated VEP amplitude in the mouse model of human chr16p11.2 micro-deletion but they also noted that plasticity and learning, in the form of stimulus-selective response potentiation (SRP) of the VEP and orientation selective behavioral habituation (OSH), respectively, are impaired in the mice. Both SRP (7) and OSH (8) are relatively easy to assay non-invasively, so there exists an intriguing opportunity to determine whether humans also display these forms of plasticity/learning. If so, this work will lay the foundation for future projects examining VEP as a potential biomarker for stratification and treatment response. In this pilot project we aim to determine in the Nelson laboratory whether the electrophysiological and behavioral phenomena of SRP and OSH, which have previously been characterized in mice, are conserved in human subjects. We will test this by using electroencephalography (EEG) to non-invasively measure VEPs over visual cortex in human participants to sine-wave gratings over consecutive days of testing. We will use a paradigm that closely parallels that of the mouse work in Mark Bear's laboratory in order to determine if there are measurable changes in VEP amplitude to familiar versus novel stimuli that bear the features of SRP. Areas of potential involvement for medical students: • They could add on a small sub-study • They could participate in data collection or other existing part of the study • They could use the data to address a new research question

Available: 03/01/15, Expires: 02/28/21

The goal of this research network is to reduce the prevalence of lifelong health impairments that are caused by toxic stress in the early years of life. The network is focused on identifying biomarkers for behavioral, autonomic, neuroendocrine, immune, and metabolic resilience to early life adversity in very young children. Areas of potential involvement for medical students: • They could add on a small sub-study • They could participate in data collection or other existing part of the study • They could use the data to address a new research question

Exploring Policy Implications of the Bucharest Early Intervention Project
Summer, 06/12/13 - 08/16/13
Effects of Institutionalized Care on Social and Academic Acclimation
Summer, 06/14/13 - 08/09/13
Perinatal Factors in Long Term Developmental Outcomes
International, 08/05/13 - 09/29/13
Aggressive Behavior in Romanian Children
Summer, 06/25/13 - 08/05/13
Effects of perinatal factors on long term developmental outcomes in children the Bucharest Early Interventional Project, Romania
International/Summer, 08/01/13 - 09/28/13
Evaluating Foster Parents' Experiences in the Bucharest Early Intervention Project (BEIP)
Summer, 06/20/14 - 08/29/14
Investigation of the Reasons for Child Abandonment in Romania within the context of the Bucharest Early Intervention Project
International, 06/15/08 - 08/10/08
The use of event related potentials as a possible marker for the development of autism spectrum disorders.
Summer, 06/18/06 - 08/11/06
Memory and executive function in children with a history of early institutionalization
Full Time, 07/01/08 - 06/30/09

The research activities and funding listed below are automatically derived from NIH ExPORTER and other sources, which might result in incorrect or missing items. Faculty can login to make corrections and additions.
  1. R34DA050289