The 6th leading cause of death in the United States is Alzheimer's Disease. Research conducted via UCLA, has pointed to a specialized curcumin that has the necessary bioavailability to cross the blood brain barrier to impact tau oligomers. This latest study abstract below is well worth the read.
Late stage intervention with curcumin reduces soluble tau oligomers and corrects cognitive and synaptic deficits
Insoluble tau and neurofibrillary tangles are hallmarks of Alzheimer's disease(AD) and persist along with cognitive deficits even after plaque reduction with anti-Abeta immunotherapy suggesting tangles are a critical AD target. However, recent studies have implicated tau oligomers as more closely associated with improved cognitive deficits after turning down the transgene in high expressing tau transgenic mice with a frontotemporal
dementia mutation. AD lacks tau mutations raising the issue of whether reducing tau oligomers with potential therapeutic agents can improve cognitive deficits post pathology in the absence of
mutant tau.
Methods: Wild type human tau transgenic mice are reported to have tangles as well as cognitive and synaptic deficits by 12 months of age. We tested the impact of late iintervention at 14-15 months (post tangles and cognitive deficits) with dietary (500 ppm)curcumin(as “Longvida”, Verdure Sciences, IN), a polyphenolic anti-inflammatory antioxidant that binds tau aggregates
and successfully treats pre-existing amyloid plaque pathology using late intervention in animal models. Morris Water Maze (MWM) was performed prior to biochemistry and ICC at 19-20 months of age.
Results: Curcumin treatment improved latency, accuracy and probe trial deficits without reducing insoluble hippocampal tau or tangles. Soluble tau oligomers detected with p422S, PHF-1 and total tau antibodies were markedly reduced by curcumin. Tau Tg dependent losses of PSD-95, NR2B and GluR1 in the detergent lysis fraction (1% Triton X-100, 0.5% SDS) were
prevented by curcumin. Tau Tg-induced elevations of PSD-95, NR2B and fyn in 2% SDSextracts of detergent were also prevented and associated with a large reduction in detergentfraction fyn.
Conclusions: Elevated soluble tau oligomers, cognitive deficits, glutamate receptor dysregulation and tau partner fyn were effectively reduced with late intervention with oral curcumin. Because reduction of tau binding partner fyn can also protect glutamate receptor dysregulation-related cognitive deficits induced by Abeta oligomers, our results suggest possible
common pathways and safe treatments for both Abeta and tau oligomer-mediated synaptic and cognitive deficits.
Link: http://www.eastonad.ucla.edu/AAICAD/AAIC2011/Cole/Frautschy-Late_stage_intervention_with_curcumin_reduces_soluble_tau_oligomers_and_corrects_cognitive_and_synaptic_deficits_ICAD2011_abstract.pdf
