Neurologists
16 years of experience
Video profile
Accepting new patients
Mid-City
UCLA -Santa Monica Neurological Assn.
1245 16th St
Ste 309
Santa Monica, CA 90404
310-319-5098
Locations and availability (3)

Education ?

Medical School Score Rankings
University of California at Los Angeles (1994)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Awards  
Selected for inclusion in the 2010 Los Angeles Magazine, Top Doctors January, 2010 Edition
Selected for inclusion in the 2010 Los Angeles Magazine, Top Do
Appointments
Ronald Reagan Ucla Medical Center
Associations
American Board of Psychiatry and Neurology

Affiliations ?

Dr. Porter is affiliated with 7 hospitals.

Hospital Affilations

Score

Rankings

  • St. John's Regional Medical Center
    1600 N Rose Ave, Oxnard, CA 93030
    • Currently 4 of 4 crosses
    Top 25%
  • UCLA Medical Center
    10833 Le Conte Ave, Los Angeles, CA 90095
    • Currently 4 of 4 crosses
    Top 25%
  • Santa Monica - UCLA Medical Center
    1250 16th St, Santa Monica, CA 90404
    • Currently 3 of 4 crosses
    Top 50%
  • Mattel Chldns Hosp. At Ucla
    10833 Le Conte Ave, Los Angeles, CA 90095
  • University of California - Ronald Reagan UCLA Medical Center
    757 Westwood Plz, Los Angeles, CA 90095
  • Santa Monica -U C L A Med Ctr, Santa Monica, Ca
  • John Muir Medical Center-Concord Campus
  • Publications & Research

    Dr. Porter has contributed to 4 publications.
    Title Frequency and Characteristics of Anxiety Among Patients with Alzheimer's Disease and Related Dementias.
    Date June 2003
    Journal The Journal of Neuropsychiatry and Clinical Neurosciences
    Excerpt

    The purpose of this study was to assess the cross-sectional prevalence and characteristics of anxiety among patients with Alzheimer's disease (AD), as compared with patients with frontotemporal dementia (FTD), patients with vascular dementia (VaD), and normal control subjects. The authors used the anxiety subscale of the Neuropsychiatric Inventory (NPI), an instrument with established reliability and validity, to compare patients. Patients were identified in a query of the UCLA Alzheimer's Disease Center database and included 115 patients with probable AD, 43 patients with VaD, 33 patients with FTD, and 40 normal, elderly control subjects. Descriptive statistics were generated, and partial correlations, controlling for Mini-Mental State Examination (MMSE) score, were performed between the anxiety subscale and other behavioral features as measured by the NPI and the Functional Activities Questionnaire (FAQ). Relationships between cognitive status (as indicated by MMSE score) and anxiety were explored. Anxiety was reported more commonly in patients with VaD and FTD than in patients with AD. These differences remained significant (P<0.01) in an analysis of variance (ANOVA) after adjusting for age, age at onset, educational level, and MMSE score. In AD, anxiety was inversely related to MMSE score (i.e., worse with more severe dementia), was more prevalent among patients with a younger age at onset (under age 65), and correlated with disability as measured by the FAQ score. These data suggest that anxiety is common among patients with diverse forms of dementia. In AD, anxiety is most common in those with more severe cognitive deterioration and an earlier age at onset.

    Title Telomere Shortening in T Cells Correlates with Alzheimer's Disease Status.
    Date March 2003
    Journal Neurobiology of Aging
    Excerpt

    Telomeres, the repeated sequences that cap chromosome ends, undergo shortening with each cell division, and therefore serve as markers of a cell's replicative history. In vivo, clonal expansion of T cells during immune responses to both foreign and autoantigens is associated with telomere shortening. To investigate possible immune alterations in Alzheimer's disease (AD) that might impact current vaccine-based therapeutic strategies, we analyzed telomere lengths in immune cell populations from AD patients. Our data show a significant telomere shortening in PBMC from AD versus controls (P=0.04). Importantly, telomere length of T cells, but not of B cells or monocytes, correlated with AD disease status, measured by Mini Mental Status Exam (MMSE) scores (P=0.025). T cell telomere length also inversely correlated with serum levels of the proinflammatory cytokine TNFalpha (a clinical marker of disease status), with the proportion of CD8+ T cells lacking expression of the CD28 costimulatory molecule, and with apoptosis. These findings suggest an immune involvement in AD pathogenesis.

    Title Immune Effects of Hormone Replacement Therapy in Post-menopausal Women.
    Date May 2001
    Journal Experimental Gerontology
    Excerpt

    Hormone replacement therapy (HRT) confers many health benefits to post-menopausal women. Despite links between estrogen and immune function prior to menopause, the immune status of women receiving HRT has not been rigorously investigated. This case-control study uses clinical laboratory assessment, flow cytometry, and functional assays to measure immune function. Participants included 27 post-menopausal women taking estrogen/progestin combinations, and 22 post-menopausal women not receiving HRT. Compared to the (-)HRT group, the (+)HRT group had more B-cells (p<0.05), higher mitogen-induced T-cell proliferation (p<0.05), and higher levels of induced TNF-alpha (p<0.05). There was a trend towards a lower proportion of CD4+ T-cells expressing the activation marker CD25+ (p<0.10). These findings represent a reversal of immune alterations associated with normal aging, suggesting that preservation or improvement of immune function may be associated with the use of HRT.

    Title Myelin Protein Expression is Increased in Lymph Nodes of Mice with Relapsing Experimental Autoimmune Encephalomyelitis.
    Date November 1997
    Journal Journal of Immunology (baltimore, Md. : 1950)
    Excerpt

    Myelin proteins had been thought to be sequestered behind the blood-brain barrier. Recently, however, myelin proteins have been found to be expressed in lymphoid tissues. The myelin basic protein (MBP) gene is embedded within a larger transcription unit called the golli-MBP gene. This larger gene encodes both the "classic" MBPs as well as the structurally related golli-MBPs. In this study, golli-MBP expression in lymph nodes was examined in four different models of relapsing experimental autoimmune encephalomyelitis (rEAE). Disease in these rEAE models was induced by the adoptive transfer of T lymphocytes specific for 18.5-kDa MBP, MBP peptide 83-102, or PLP peptide 139-151 in the SJL/J mouse and the adoptive transfer of T lymphocytes specific for MBP peptide Ac1-9 in the (SJL/J x PL/J)F1 mouse. In all four models, expression of golli-MBP BG21 mRNA was increased two- to fivefold in lymph nodes of mice 45 to 60 days post-transfer. Immunohistochemical analysis indicated that expression occurred principally in macrophages within lymph nodes. Endogenous golli-MBP epitopes within lymph node cells stimulated "classic" MBP 1-44-specific T lymphocytes, and this stimulatory ability resided within the adherent lymph node cell population. An increase in myelin protein expression within lymph nodes during rEAE has implications with regard to intra- and intermolecular epitope spreading. This is the first report describing an increase in target autoantigen expression within lymphoid tissue during an autoimmune disease.


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