<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03038334</url>
  </required_header>
  <id_info>
    <org_study_id>PR02TCR011-17</org_study_id>
    <nct_id>NCT03038334</nct_id>
  </id_info>
  <brief_title>Magnesium Sulfate for the Improvement of Cognition in Patients With Alzheimer Disease</brief_title>
  <official_title>Magnesium Sulfate for the Improvement of Cognition in Patients With Alzheimer Disease</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Metabolic Therapy Inc.</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Metabolic Therapy Inc.</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      This study is to examine the possible effect of supplementing Magnesium sulfate on patients&#xD;
      with Alzheimer Disease (AD) in controlling or reducing the amount of amyloid present in the&#xD;
      brain, and increasing cognitive ability in individuals that have amyloid deposits.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Recent findings suggest magnesium may be effective in ameliorating symptoms in an Alzheimer's&#xD;
      disease-like pathological progression by reducing Aβ-plaque, thus preventing synapse loss and&#xD;
      memory decline in transgenic mice. Common forms include magnesium sulfate.&#xD;
&#xD;
      As a nutritional adjunct in hyperalimentation, the precise mechanism of action for magnesium&#xD;
      is uncertain. Predominant deficiency effects are neurological, e.g., muscle irritability,&#xD;
      clonic twitching and tremors. Hypocalcemia and hypokalemia often follow low serum levels of&#xD;
      magnesium. While there are large stores of magnesium present intracellularly and in the bones&#xD;
      of adults, these stores often are not mobilized sufficiently to maintain plasma levels.&#xD;
      Parenteral magnesium therapy repairs the plasma deficit and causes deficiency symptoms and&#xD;
      signs to cease.&#xD;
&#xD;
      To provide a comprehensive clinical evaluation of the effects of Magnesium sulfate in AD&#xD;
      patients, this study is designed to assess the impact of magnesium sulfate on amyloid plaque&#xD;
      to generate valuable data on clinical utility for the use of diagnostic algorithms and&#xD;
      foundation for the development of possible treatment.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Not yet recruiting</last_known_status>
  <start_date type="Anticipated">February 20, 2017</start_date>
  <completion_date type="Anticipated">October 20, 2019</completion_date>
  <primary_completion_date type="Anticipated">August 20, 2019</primary_completion_date>
  <phase>N/A</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>N/A</allocation>
    <intervention_model>Single Group Assignment</intervention_model>
    <primary_purpose>Treatment</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Change in amyloid deposit</measure>
    <time_frame>Baseline to 12 weeks</time_frame>
    <description>Amyloid deposit measure will mean change from baseline to 12 weeks in Florbetapir cortical-to-cerebellar ratio averaged across 6 regions of interest (frontal, temporal, parietal, anterior cingulate, posterior cingulate, and precuneus).Brain imaging focusing on the following anatomical regions: medial temporal region (including hippocampus andentorhinal cortex), prefrontal cortex, parietotemporal cortex, posterior cingulate cortex.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Cognitive Function</measure>
    <time_frame>Baseline to 12 weeks</time_frame>
    <description>Composite scores for the four following cognitive areas include: 1) memory composite score 2) attention composite score 3) learning composite score 4) executive function composite score</description>
  </secondary_outcome>
  <number_of_arms>1</number_of_arms>
  <enrollment type="Anticipated">100</enrollment>
  <condition>Alzheimer Disease</condition>
  <arm_group>
    <arm_group_label>Magnesium sulfate</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>All participants will apply magnesium sulfate transdermally a total of 250mg equivalent to 2 mEq every four hours per day for 90 days.</description>
  </arm_group>
  <intervention>
    <intervention_type>Dietary Supplement</intervention_type>
    <intervention_name>Magnesium sulfate</intervention_name>
    <description>Transdermal application of Magnesium sulfate 250mg every four hours per day for 90 days.</description>
    <arm_group_label>Magnesium sulfate</arm_group_label>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Outpatients with a diagnosis of Alzheimer's disease.&#xD;
&#xD;
          -  Exhibiting an onset and progression of cognitive dysfunction during at least 3 months&#xD;
             prior to the screening period.&#xD;
&#xD;
          -  Subject or representative is willing to sign the consent for prior to enrollment into&#xD;
             the study and to participate in all aspects of the study. Prospective subject must&#xD;
             give verbal assent if unable to sign written consent.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Patients with neurodegenerative diseases other than Alzheimer's disease.&#xD;
&#xD;
          -  Patients with cognitive dysfunction due to cerebral damage resulting from a lack of&#xD;
             oxygen, a brain injury, etc.&#xD;
&#xD;
          -  Patients with clinically significant cardiovascular disease.&#xD;
&#xD;
          -  Patients with history of clinically-evident stroke.&#xD;
&#xD;
          -  Patients with history of cancer in the last 5 years.&#xD;
&#xD;
          -  Patients with clinically-significant systemic illness that may affect safety or&#xD;
             completion of the study.&#xD;
&#xD;
          -  Currently taking any medications that are known to interact with magnesium.&#xD;
&#xD;
          -  Currently taking antibiotics as the study product may reduce the absorption of&#xD;
             antibiotics. A washout period of 2 weeks is allowed.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>50 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Andreana Haley, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University of Texas - Austin</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Dewey C Brown II, PhD</last_name>
    <phone>2145174004</phone>
  </overall_contact>
  <verification_date>January 2017</verification_date>
  <study_first_submitted>January 26, 2017</study_first_submitted>
  <study_first_submitted_qc>January 27, 2017</study_first_submitted_qc>
  <study_first_posted type="Estimate">January 31, 2017</study_first_posted>
  <last_update_submitted>January 27, 2017</last_update_submitted>
  <last_update_submitted_qc>January 27, 2017</last_update_submitted_qc>
  <last_update_posted type="Estimate">January 31, 2017</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Alzheimer Disease</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Magnesium Sulfate</mesh_term>
  </intervention_browse>
  <patient_data>
    <sharing_ipd>Undecided</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03038334
org study id: PR02TCR011-17
nct id: NCT03038334
lead sponsor: 
has dmc: Yes
is fda regulated drug: No
is fda regulated device: No
This study is to examine the possible effect of supplementing Magnesium sulfate on patients
      with Alzheimer Disease (AD) in controlling or reducing the amount of amyloid present in the
      brain, and increasing cognitive ability in individuals that have amyloid deposits.
Recent findings suggest magnesium may be effective in ameliorating symptoms in an Alzheimer's
      disease-like pathological progression by reducing Aβ-plaque, thus preventing synapse loss and
      memory decline in transgenic mice. Common forms include magnesium sulfate.

      As a nutritional adjunct in hyperalimentation, the precise mechanism of action for magnesium
      is uncertain. Predominant deficiency effects are neurological, e.g., muscle irritability,
      clonic twitching and tremors. Hypocalcemia and hypokalemia often follow low serum levels of
      magnesium. While there are large stores of magnesium present intracellularly and in the bones
      of adults, these stores often are not mobilized sufficiently to maintain plasma levels.
      Parenteral magnesium therapy repairs the plasma deficit and causes deficiency symptoms and
      signs to cease.

      To provide a comprehensive clinical evaluation of the effects of Magnesium sulfate in AD
      patients, this study is designed to assess the impact of magnesium sulfate on amyloid plaque
      to generate valuable data on clinical utility for the use of diagnostic algorithms and
      foundation for the development of possible treatment.
allocation: N/A
intervention model: Single Group Assignment
primary purpose: Treatment
masking: None (Open Label)
measure: Change in amyloid deposit
time frame: Baseline to 12 weeks
description: Amyloid deposit measure will mean change from baseline to 12 weeks in Florbetapir cortical-to-cerebellar ratio averaged across 6 regions of interest (frontal, temporal, parietal, anterior cingulate, posterior cingulate, and precuneus).Brain imaging focusing on the following anatomical regions: medial temporal region (including hippocampus andentorhinal cortex), prefrontal cortex, parietotemporal cortex, posterior cingulate cortex.
measure: Cognitive Function
time frame: Baseline to 12 weeks
description: Composite scores for the four following cognitive areas include: 1) memory composite score 2) attention composite score 3) learning composite score 4) executive function composite score
arm group label: Magnesium sulfate
arm group type: Experimental
description: All participants will apply magnesium sulfate transdermally a total of 250mg equivalent to 2 mEq every four hours per day for 90 days.
intervention type: Dietary Supplement
intervention name: Magnesium sulfate
description: Transdermal application of Magnesium sulfate 250mg every four hours per day for 90 days.
arm group label: Magnesium sulfate
criteria: 
gender: All
minimum age: 50 Years
maximum age: N/A
healthy volunteers: No
last name: Andreana Haley, PhD
role: Principal Investigator
affiliation: University of Texas - Austin
last name: Dewey C Brown II, PhD
phone: 2145174004
responsible party type: Sponsor
mesh term: Alzheimer Disease
mesh term: Magnesium Sulfate
sharing ipd: Undecided