Bio

Bio


Dr. Alesha Heath is a Postdoctoral Scholar at Psychiatry and Behavioral Sciences at Stanford School of Medicine and the MIRECC the VA Palo Alto. She earned her PhD from the University of Western Australia and Sorbonne University.

Dr. Heath's research has been primarily focused on the mechanisms and applications of brain stimulation therapies, in particular repetitive transcranial magnetic stimulation. Her research involves both basic and clinical components with the aim of improving the efficacy of these therapies for the treatment of disorders such as depression and Alzheimer's disease.

Professional Education


  • Doctor of Philosophy, Sorbonne University (2019)
  • Doctor of Philosophy, University Of Western Australia (2019)
  • Bachelor of Science, University Of Western Australia (2015)

Stanford Advisors


Publications

All Publications


  • Sleep-wake disorders in Alzheimer's disease: further genetic analyses in relation to objective sleep measures. International psychogeriatrics Yesavage, J. A., Noda, A., Heath, A., McNerney, M. W., Domingue, B. W., Hernandez, Y., Benson, G., Hallmayer, J., O'Hara, R., Williams, L. M., Goldstein-Piekarski, A. N., Zeitzer, J. M., Fairchild, J. K. 2019: 1–7

    Abstract

    This paper presents updated analyses on the genetic associations of sleep disruption in individuals with Alzheimer's disease (AD). We published previously a study of the association between single nucleotide polymorphisms (SNPs) found in eight genes related to circadian rhythms and objective measures of sleep-wake disturbances in 124 individuals with AD. Here, we present new relevant analyses using polygenic risk scores (PRS) and variable number tandem repeats (VNTRs) enumerations. PRS were calculated using the genetic data from the original participants and relevant genome wide association studies (GWAS). VNTRs for the same circadian rhythm genes studied with SNPs were obtained from a separate cohort of participants using whole genome sequencing (WGS). Objectively (wrist actigraphy) determined wake after sleep onset (WASO) was used as a measure of sleep disruption. None of the PRS were associated with sleep disturbance. Computer analyses using VNTRseek software generated a total of 30 VNTRs for the circadian-related genes but none appear relevant to our objective sleep measure. In addition, of 71 neurotransmitter function-related genes, 29 genes had VNTRs that differed from the reference VNTR, but it was not clear if any of these might affect circadian function in AD patients. Although we have not found in either the current analyses or in our previous published analyses of SNPs any direct linkages between identified genetic factors and WASO, research in this area remains in its infancy.

    View details for DOI 10.1017/S1041610219001777

    View details for PubMedID 31739820

  • rTMS for the treatment of Alzheimer's disease: where should we be stimulating? EXPERT REVIEW OF NEUROTHERAPEUTICS Heath, A., Taylor, J. L., McNerney, M. 2018; 18 (12): 903–5

    View details for PubMedID 30350733

  • Medium- and high-intensity rTMS reduces psychomotor agitation with distinct neurobiologic mechanisms TRANSLATIONAL PSYCHIATRY Heath, A., Lindberg, D. R., Makowiecki, K., Gray, A., Asp, A. J., Rodger, J., Choi, D., Croarkin, P. E. 2018; 8: 126

    Abstract

    Definitive data are lacking on the mechanism of action and biomarkers of repetitive transcranial magnetic stimulation (rTMS) for the treatment of depression. Low-intensity rTMS (LI-rTMS) has demonstrated utility in preclinical models of rTMS treatments but the effects of LI-rTMS in murine models of depression are unknown. We examined the behavioral and neurobiologic changes in olfactory bulbectomy (OB) mice with medium-intensity rTMS (MI-rTMS) treatment and fluoxetine hydrochloride. We then compared 10-Hz rTMS sessions for 3 min at intensities (measured at the cortical surface) of 4 mT (LI-rTMS), 50 mT (medium-intensity rTMS [MI-rTMS]), or 1 T (high-intensity rTMS [HI-rTMS]) 5 days per week over 4 weeks in an OB model of agitated depression. Behavioral effects were assessed with forced swim test; neurobiologic effects were assessed with brain levels of 5-hydroxytryptamine, brain-derived neurotrophic factor (BDNF), and neurogenesis. Peripheral metabolomic changes induced by OB and rTMS were monitored through enzyme-linked immunosorbent assay and ultrapressure liquid chromatography-driven targeted metabolomics evaluated with ingenuity pathway analysis (IPA). MI-rTMS and HI-rTMS attenuated psychomotor agitation but only MI-rTMS increased BDNF and neurogenesis levels. HI-rTMS normalized the plasma concentration of α-amino-n-butyric acid and 3-methylhistidine. IPA revealed significant changes in glutamine processing and glutamate signaling in the OB model and following MI-rTMS and HI-rTMS treatment. The present findings suggest that MI-rTMS and HI-rTMS induce differential neurobiologic changes in a mouse model of agitated depression. Further, α-amino-n-butyric acid and 3-methylhistidine may have utility as biomarkers to objectively monitor the response to rTMS treatment of depression.

    View details for DOI 10.1038/s41398-018-0129-3

    View details for Web of Science ID 000438104100001

    View details for PubMedID 29976924

    View details for PubMedCentralID PMC6033856

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