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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.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Magnesium sulfate | Experimental | All participants will apply magnesium sulfate transdermally a total of 250mg equivalent to 2 mEq every four hours per day for 90 days. |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| Magnesium sulfate | Dietary Supplement | Transdermal application of Magnesium sulfate 250mg every four hours per day for 90 days. |
|
| Measure | Description | Time Frame |
|---|---|---|
| Change in amyloid deposit | 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. | Baseline to 12 weeks |
| Measure | Description | Time Frame |
|---|---|---|
| Cognitive Function | 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 | Baseline to 12 weeks |
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Inclusion Criteria:
Exclusion Criteria:
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| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| Dewey C Brown II, PhD | Contact | 2145174004 |
| Name | Affiliation | Role |
|---|---|---|
| Andreana Haley, PhD | University of Texas at Austin | Principal Investigator |
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| ID | Term |
|---|---|
| D000544 | Alzheimer Disease |
| ID | Term |
|---|---|
| D003704 | Dementia |
| D001927 | Brain Diseases |
| D002493 | Central Nervous System Diseases |
| D009422 | Nervous System Diseases |
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| ID | Term |
|---|---|
| D008278 | Magnesium Sulfate |
| ID | Term |
|---|---|
| D017616 | Magnesium Compounds |
| D007287 | Inorganic Chemicals |
| D013431 | Sulfates |
| D013464 | Sulfuric Acids |
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| D024801 |
| Tauopathies |
| D019636 | Neurodegenerative Diseases |
| D019965 | Neurocognitive Disorders |
| D001523 | Mental Disorders |
| D013456 |
| Sulfur Acids |
| D013457 | Sulfur Compounds |