Ron-
I often find that a bite to eat will kick me on. I've always marked it off to glucose levels but I have no other sugar problems so that may be entirely wrong.

I do think that your loyalty to curcumin has paid off for you. A couple studies of note:


1. Acta Neuropathol. 2008 Apr;115(4):479-89. Epub 2008 Jan 10.

Curcumin inhibits aggregation of alpha-synuclein.

Pandey N, Strider J, Nolan WC, Yan SX, Galvin JE.

Department of Anatomy and Neurobiology, Washington University School of Medicine,
St Louis, MO 63110, USA.

Aggregation of amyloid-beta protein (Abeta) is a key pathogenic event in
Alzheimer's disease (AD). Curcumin, a constituent of the Indian spice Turmeric is
structurally similar to Congo Red and has been demonstrated to bind Abeta amyloid
and prevent further oligomerization of Abeta monomers onto growing amyloid
beta-sheets. Reasoning that oligomerization kinetics and mechanism of amyloid
formation are similar in Parkinson's disease (PD) and AD, we investigated the
effect of curcumin on alpha-synuclein (AS) protein aggregation. In vitro model of
AS aggregation was developed by treatment of purified AS protein (wild-type) with
1 mM Fe3+ (Fenton reaction). It was observed that the addition of curcumin
inhibited aggregation in a dose-dependent manner and increased AS solubility. The
aggregation-inhibiting effect of curcumin was next investigated in cell culture
utilizing catecholaminergic SH-SY5Y cell line. A model system was developed in
which the red fluorescent protein (DsRed2) was fused with A53T mutant of AS and
its aggregation examined under different concentrations of curcumin. To estimate
aggregation in an unbiased manner, a protocol was developed in which the images
were captured automatically through a high-throughput cell-based screening
microscope. The obtained images were processed automatically for aggregates
within a defined dimension of 1-6 microm. Greater than 32% decrease in mutant
alpha-synuclein aggregation was observed within 48 h subsequent to curcumin
addition. Our data suggest that curcumin inhibits AS oligomerization into higher
molecular weight aggregates and therefore should be further explored as a
potential therapeutic compound for PD and related disorders.


PMID: 18189141 [PubMed - indexed for MEDLINE]



1. BMC Neurosci. 2010 Apr 30;11:57.

Curcumin reduces alpha-synuclein induced cytotoxicity in Parkinson's disease cell
model.

Wang MS, Boddapati S, Emadi S, Sierks MR.

Department of Chemical Engineering, Arizona State University, Tempe, AZ
85287-6006, USA.

BACKGROUND: Overexpression and abnormal accumulation of aggregated
alpha-synuclein (alphaS) have been linked to Parkinson's disease (PD) and other
synucleinopathies. alphaS can misfold and adopt a variety of morphologies but
recent studies implicate oligomeric forms as the most cytotoxic species. Both
genetic mutations and chronic exposure to neurotoxins increase alphaS aggregation
and intracellular reactive oxygen species (ROS), leading to mitochondrial
dysfunction and oxidative damage in PD cell models. RESULTS: Here we show that
curcumin can alleviate alphaS-induced toxicity, reduce ROS levels and protect
cells against apoptosis. We also show that both intracellular overexpression of
alphaS and extracellular addition of oligomeric alphaS increase ROS which induces
apoptosis, suggesting that aggregated alphaS may induce similar toxic effects
whether it is generated intra- or extracellulary. CONCLUSIONS: Since curcumin is
a natural food pigment that can cross the blood brain barrier and has widespread
medicinal uses, it has potential therapeutic value for treating PD and other
neurodegenerative disorders.


PMCID: PMC2879277
PMID: 20433710 [PubMed - indexed for MEDLINE]