lack of support

Curcumin is shown to impact several different pathways of neuroprotection, however clinical trials have not shown positive results, due to the poor bioavailability of curcumin. This study is designed to determine efficacy and safety of high-bioavailability curcumin formulation (Longvida) in subjects with Alzheimer's disease.

Curcumin is a polyphenolic molecule that comprises approximately 3-5% of turmeric (Curcuma longa) root, giving the spice its characteristic yellow color. Because of its anti-inflammatory, anti-amyloid, and antioxidant properties, curcumin has shown positive effects in animal models of Alzheimer's disease (AD). However, a six month human study was conducted with unformulated curcumin showing insignificant trends, due to limited bioavailability and brain permeability of unformulated curcumin. In animal models of AD, oral dosing of solid-lipid curcumin particle (SLCP or Longvida) significantly reduced memory deficit and impacted biomarkers better than unformulated curcumin. This study is to determine the potential efficacy and safety of highly absorbed SLCP curcumin in subjects with AD.

Inclusion Criteria:

• Male or Female age ≥ 50.
• Diagnosed with probable AD using NINDS-ADRDA research criteria. MMSE score ≥5 and ≤20.
• No history of significant psychiatric or non-AD neurological disease.
• An available caregiver to monitor and administer medication and to accompany the subject to every clinical visit.
• On stable doses of concomitant medications for at least one month prior to starting study medication.

Exclusion Criteria:

• Current or recent major psychiatric illness that meets DSM-IV criteria (i.e. bipolar disorder, schizophrenia).
• Significant uncontrolled systemic illness (i.e. chronic renal failure, chronic liver disease, poorly controlled diabetes, or poorly controlled congestive heart failure).
• Recent history of gastrointestinal bleeding or ulceration.
• Alcoholism or substance abuse within the past year per DSM-IV criteria.
• Familial, autosomal dominant Alzheimer's disease due to a mutation in a known gene (Presenilin-1, Presenilin-2, or Amyloid Precursor Protein).