Demetrius M. Maraganore, M.D.

Demetrius M. Maraganore, M.D.

Demetrius M. Maraganore, M.D.

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Personal Bio

Treatment Philosophy

It is my core value, and the core value of our Department of Neurology, that the needs of the patient come first. I believe that as the leaders in our field, it is our responsibility to provide tomorrow's healthcare today.

Personal Interests

My personal interests are to develop methods to predict, prevent, and halt neurological diseases, through the application of molecular prognostic and therapeutic approaches; and to lead the region's pre-eminent providers of neurological care.

Conditions & Procedures

Conditions

Parkinsonism, Parkinson's Disease (PD), Tremors

General Information

Gender

Male

Affiliation

NorthShore Medical Group

Academic Rank

Clinical Professor

Languages

English, Greek, Italian

Board Certified

Neurology

Clinical Service

Education, Training & Fellowships

Medical School

Northwestern Feinberg School of Medicine, 1985

Internship

Mayo School of Graduate Medical Education, 1986

Residency

Mayo School of Graduate Medical Education, 1989

Fellowship

National Hospital for Neurology and Neurosurgery, 1990

Locations

A

NorthShore Medical Group

2180 Pfingsten Rd.
Suite 2000
Glenview, IL 60026
847.570.2570 847.657.5708 fax Get Directions This location is wheelchair accessible.

Insurance

Commercial Plans
  • Aetna Choice POS (Open Access) and POS II (Open Access)
  • Aetna Elect Choice EPO and EPO Open Access
  • Aetna Health Network Options
  • Aetna HMO (including Open Access)
  • Aetna Managed Choice (Open Access)
  • Aetna Managed Choice POS
  • Aetna Open Access Aetna Select (Aetna HealthFund)
  • Aetna Open Access Elect Choice EPO (Aetna HealthFund)
  • Aetna Open Access Managed Choice POS (Aetna HealthFund)
  • Aetna Open Choice PPO
  • Aetna Open Choice PPO (Aetna HealthFund)
  • Aetna Premier Care Network
  • Aetna QPOS
  • Aetna Select
  • Aetna Select (Open Access)
  • Beechstreet PPO Network
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Advantage
    Verify PCP Participation
  • Blue Cross Blue Shield HMOI
  • Cigna HMO
  • Cigna LocalPlus
  • Cigna Open Access Plus (OAP)
  • Cigna Open Access Plus with CareLink (OAPC)
  • Cigna POS
  • Cigna PPO
  • Cofinity PPO (an Aetna Company)
  • Coventry Health Care Elect Choice EPO
  • Coventry Health Care First Health PPO
  • Galaxy Health PPO Network
  • Great West PPO/POS
  • Healthcare's Finest Network (HFN)
  • Humana - All Commercial Plans (including Choice Care)
  • Humana - NorthShore Complete Care
  • Humana/ChoiceCare Network PPO
  • Medicare
  • Multiplan and PHCS PPO Network (Including PHCS Savility)
  • NorthShore Employee Network
  • Preferred Plan PPO
  • Three Rivers Provider PPO Network (TRPN)
  • Tricare
  • Unicare
  • United Healthcare - All Commercial Plans
    Not Contracted United Healthcare Core
    Not Contracted United Healthcare Navigate
Exchange Plans
  • Not Contracted Aetna
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Precision
    Verify PCP Participation
  • Not Contracted Coventry
  • Humana National
  • Land of Lincoln - All Products
  • Not Contracted United Healthcare Compass
Medicaid
  • Illinois Department of Public Aid (IDPA)
  • Illinicare ICP
  • Community Care Partners
Medicare Advantage Plans
  • Aetna Medicare (SM) Plan (HMO/Open Access HMO)
  • Aetna Medicare (SM) Plan (PPO)
  • Blue Cross Blue Shield Medicare Advantage PPO Plan
  • Cigna-HealthSpring Advantage HMO
  • Cigna-HealthSpring Premier HMO-POS
  • Cigna-HealthSpring Primary HMO
  • Humana Gold Plus HMO
  • Humana Gold Plus PFFS
  • HumanaChoice PPO
  • United Healthcare - All Medicare Plans
Medicare Medicaid Alignment Initiative (MMAI) Plans
  • Blue Cross Blue Shield Community
  • HealthSpring
  • Humana
  • Illinicare Health Plan
  • Meridian Complete

Publications

  • Role for the microtubule-associated protein tau variant p.A152T in risk of α-synucleinopathies.

    Neurology 2015 Sep 2

    Authors: Labbé C,
    Abstract
    To assess the importance of MAPT variant p.A152T in the risk of synucleinopathies.
    In this case-control study, we screened a large global series of patients and controls, and assessed associations between p.A152T and disease risk. We included 3,229 patients with clinical Parkinson disease (PD), 442 with clinical dementia with Lewy bodies (DLB), 181 with multiple system atrophy (MSA), 832 with pathologically confirmed Lewy body disease (LBD), and 2,456 healthy controls.
    The minor allele frequencies (MAF) in clinical PD cases (0.28%) and in controls (0.2%) were not found to be significantly different (odds ratio [OR] 1.37, 95% confidence interval [CI] 0.63-2.98, p = 0.42). However, a significant association was observed with clinical DLB (MAF 0.68%, OR 5.76, 95% CI 1.62-20.51, p = 0.007) and LBD (MAF 0.42%, OR 3.55, 95% CI 1.04-12.17, p = 0.04). Additionally, p.A152T was more common in patients with MSA compared to controls (MAF 0.55%, OR 4.68, 95% CI 0.85-25.72, p = 0.08) but this was not statistically significant and therefore should be interpreted with caution.
    Overall, our findings suggest that MAPT p.A152T is a rare low penetrance variant likely associated with DLB that may be influenced by coexisting LBD and AD pathology. Given the rare nature of the variant, further studies with greater sample size are warranted and will help to fully explain the role of p.A152T in the pathogenesis of the synucleinopathies.
    PMID: 26333800 [PubMed - as supplied by publisher]
  • Clinically meaningful parameters of progression and long-term outcome of Parkinson disease: An international consensus statement.

    Parkinsonism & related disorders 2015 Jul

    Authors: Puschmann A,
    Abstract
    Parkinson disease (PD) is associated with a clinical course of variable duration, severity, and a combination of motor and non-motor features. Recent PD research has focused primarily on etiology rather than clinical progression and long-term outcomes. For the PD patient, caregivers, and clinicians, information on expected clinical progression and long-term outcomes is of great importance. Today, it remains largely unknown what factors influence long-term clinical progression and outcomes in PD; recent data indicate that the factors that increase the risk to develop PD differ, at least partly, from those that accelerate clinical progression and lead to worse outcomes. Prospective studies will be required to identify factors that influence progression and outcome. We suggest that data for such studies is collected during routine office visits in order to guarantee high external validity of such research. We report here the results of a consensus meeting of international movement disorder experts from the Genetic Epidemiology of Parkinson's Disease (GEO-PD) consortium, who convened to define which long-term outcomes are of interest to patients, caregivers and clinicians, and what is presently known about environmental or genetic factors influencing clinical progression or long-term outcomes in PD. We propose a panel of rating scales that collects a significant amount of phenotypic information, can be performed in the routine office visit and allows international standardization. Research into the progression and long-term outcomes of PD aims at providing individual prognostic information early, adapting treatment choices, and taking specific measures to provide care optimized to the individual patient's needs.
    PMID: 25952959 [PubMed - as supplied by publisher]
  • Nicholas A. Vick, MD (1939–2014).

    Neurology 2015 Feb 10

    Authors: Theuns J,
    Abstract
    The objective of this study is to clarify the role of (G4C2)n expansions in the etiology of Parkinson disease (PD) in the worldwide multicenter Genetic Epidemiology of Parkinson's Disease (GEO-PD) cohort.
    C9orf72 (G4C2)n repeats were assessed in a GEO-PD cohort of 7,494 patients diagnosed with PD and 5,886 neurologically healthy control individuals ascertained in Europe, Asia, North America, and Australia.
    A pathogenic (G4C2)n>60 expansion was detected in only 4 patients with PD (4/7,232; 0.055%), all with a positive family history of neurodegenerative dementia, amyotrophic lateral sclerosis, or atypical parkinsonism, while no carriers were detected with typical sporadic or familial PD. Meta-analysis revealed a small increase in risk of PD with an increasing number of (G4C2)n repeats; however, we could not detect a robust association between the C9orf72 (G4C2)n repeat and PD, and the population attributable risk was low.
    Together, these findings indicate that expansions in C9orf72 do not have a major role in the pathogenesis of PD. Testing for C9orf72 repeat expansions should only be considered in patients with PD who have overt symptoms of frontotemporal lobar degeneration/amyotrophic lateral sclerosis or apparent family history of neurodegenerative dementia or motor neuron disease.
    PMID: 25811061 [PubMed - as supplied by publisher]
  • Does α-synuclein have a dual and opposing effect in preclinical vs. clinical Parkinson's disease?

    Parkinsonism & related disorders 2014 Jun

    Authors: Markopoulou K,
    Abstract
    α-Synuclein gene (SNCA) multiplications cause familial parkinsonism and allele-length polymorphisms within the SNCA dinucleotide repeat REP1 increase the risk for developing Parkinson's disease (PD). Since SNCA multiplications increase SNCA expression, and REP1 genotypes that increase the risk of developing PD show increased SNCA expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce SNCA expression. We conducted an observational study of 1098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced SNCA expression are associated with better motor and cognitive outcomes. We evaluated the association of REP1 genotypes with survival free of Hoehn and Yahr stages 4 or 5 (motor outcome) and of Modified Telephone Interview for Cognitive Status score ≤27 or Alzheimer's Disease Dementia Screening Interview score ≥2 (cognitive outcome). Median disease duration at baseline was 3.3 years and median lag time from baseline to follow-up was 7.8 years. Paradoxically, REP1 genotypes associated with increased risk of developing PD and increased SNCA expression were associated with better motor (HR = 0.87, p = 0.046, covariate-adjusted age-scale analysis; HR = 0.85, p = 0.020, covariate-adjusted time-scale analysis) and cognitive outcomes (HR = 0.90, p = 0.12, covariate-adjusted age-scale analysis; HR = 0.85, p = 0.023, covariate-adjusted time-scale analysis). Our findings raise the possibility that SNCA has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target SNCA expression.
    PMID: 24656894 [PubMed - as supplied by publisher]
  • Alpha-synuclein repeat variants and survival in Parkinson's disease.

    Movement disorders : official journal of the Movement Disorder Society 2014 Jul

    Authors: Chung SJ,
    Abstract
    To determine whether α-synuclein dinucleotide repeat (REP1) genotypes are associated with survival in Parkinson's disease (PD).
    Investigators from the Genetic Epidemiology of Parkinson's Disease Consortium provided REP1 genotypes and baseline and follow-up clinical data for cases. The primary outcome was time to death. Cox proportional hazards regression models were used to assess the association of REP1 genotypes with survival.
    Twenty-one sites contributed data for 6,154 cases. There was no significant association between α-synuclein REP1 genotypes and survival in PD. However, there was a significant association between REP1 genotypes and age at onset of PD (hazard ratio: 1.06; 95% confidence interval: 1.01-1.10; P value = 0.01).
    In our large consortium study, α-synuclein REP1 genotypes were not associated with survival in PD. Further studies of α-synuclein's role in disease progression and long-term outcomes are needed.
    PMID: 24578302 [PubMed - as supplied by publisher]
  • Protective effect of LRRK2 p.R1398H on risk of Parkinson's disease is independent of MAPT and SNCA variants.

    Neurobiology of aging 2014 Jan

    Authors: Heckman MG,
    Abstract
    The best validated susceptibility variants for Parkinson's disease are located in the α-synuclein (SNCA) and microtubule-associated protein tau (MAPT) genes. Recently, a protective p.N551K-R1398H-K1423K haplotype in the leucine-rich repeat kinase 2 (LRRK2) gene was identified, with p.R1398H appearing to be the most likely functional variant. To date, the consistency of the protective effect of LRRK2 p.R1398H across MAPT and SNCA variant genotypes has not been assessed. To address this, we examined 4 SNCA variants (rs181489, rs356219, rs11931074, and rs2583988), the MAPT H1-haplotype-defining variant rs1052553, and LRRK2 p.R1398H (rs7133914) in Caucasian (n = 10,322) and Asian (n = 2289) series. There was no evidence of an interaction of LRRK2 p.R1398H with MAPT or SNCA variants (all p ≥ 0.10); the protective effect of p.R1398H was observed at similar magnitude across MAPT and SNCA genotypes, and the risk effects of MAPT and SNCA variants were observed consistently for LRRK2 p.R1398H genotypes. Our results indicate that the association of LRRK2 p.R1398H with Parkinson's disease is independent of SNCA and MAPT variants, and vice versa, in Caucasian and Asian populations.
    PMID: 23962496 [PubMed - as supplied by publisher]
  • Population-specific frequencies for LRRK2 susceptibility variants in the Genetic Epidemiology of Parkinson's Disease (GEO-PD) Consortium.

    Movement disorders : official journal of the Movement Disorder Society 2013 Oct

    Authors: Heckman MG,
    Abstract
    Variants within the leucine-rich repeat kinase 2 gene are recognized as the most frequent genetic cause of Parkinson's disease. Leucine-rich repeat kinase 2 variation related to disease susceptibility displays many features that reflect the nature of complex, late-onset sporadic disorders like Parkinson's disease.
    The Genetic Epidemiology of Parkinson's Disease Consortium recently performed the largest genetic association study for variants in the leucine-rich repeat kinase 2 gene across 23 different sites in 15 countries.
    Herein, we detail the allele frequencies for the novel risk factors (p.A419V and p.M1646T) and the protective haplotype (p.N551K-R1398H-K1423K) nominated in the original publication. Simple population allele frequencies not only can provide insight into the clinical relevance of specific variants but also can help genetically define patient groups.
    Establishing individual patient-based genomic susceptibility profiles that incorporate both risk factors and protective factors will determine future diagnostic and treatment strategies.
    PMID: 23913756 [PubMed - as supplied by publisher]
  • Genetic susceptibility loci, environmental exposures, and Parkinson's disease: a case-control study of gene-environment interactions.

    Parkinsonism & related disorders 2013 Jun

    Authors: Chung SJ,
    Abstract
    Prior studies causally linked mutations in SNCA, MAPT, and LRRK2 genes with familial Parkinsonism. Genome-wide association studies have demonstrated association of single nucleotide polymorphisms (SNPs) in those three genes with sporadic Parkinson's disease (PD) susceptibility worldwide. Here we investigated the interactions between SNPs in those three susceptibility genes and environmental exposures (pesticides application, tobacco smoking, coffee drinking, and alcohol drinking) also associated with PD susceptibility.
    Pairwise interactions between environmental exposures and 18 variants (16 SNPs and two variable number tandem repeats, or "VNTRs") in SNCA, MAPT and LRRK2, were investigated using data from 1098 PD cases from the upper Midwest, USA and 1098 matched controls. Environmental exposures were assessed using a validated telephone interview script.
    Five pairwise interactions had uncorrected P-values < 0.05. These included pairings of pesticides × SNCA rs3775423 or MAPT rs4792891, coffee drinking × MAPT H1/H2 haplotype or MAPT rs16940806, and alcohol drinking × MAPT rs2435211. None of these interactions remained significant after Bonferroni correction. Secondary analyses in strata defined by type of control (sibling or unrelated), sex, or age at onset of the case also did not identify significant interactions after Bonferroni correction.
    This study documented limited pairwise interactions between established genetic and environmental risk factors for PD; however, the associations were not significant after correction for multiple testing.
    PMID: 23507417 [PubMed - as supplied by publisher]

In the News

Aug 2015

Jul 2014

Social Media

Featured Videos

Drs. Demetrius Maraganore and Julian Bailes discuss the innovative research being done at the NorthShore Neurological Institute.

Drs. Demetrius Maraganore and Julian Bailes discuss the innovative research being done at the NorthShore Neurological Institute.

NorthShore Neurological Institute - Treatments: Doctors Bailes, Alleva & Maraganore (Neurology)

NorthShore Neurological Institute - Treatments: Doctors Bailes, Alleva & Maraganore (Neurology)

NorthShore Neurological Institute - Centers & Programs: Doctors Bailes, Alleva & Maraganore (Neurology)

NorthShore Neurological Institute - Centers & Programs: Doctors Bailes, Alleva & Maraganore (Neurology)

NorthShore Neurological Institute: Doctors Bailes, Alleva & Maraganore (Neurology)

NorthShore Neurological Institute: Doctors Bailes, Alleva & Maraganore (Neurology)

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