Research published this month by researchers at the University of California Santa Barbara attributes protective effects to the common household spice, cinnamon. The paper, in The Journal of Alzheimer’s Disease, discussed a possible role for two components of cinnamon: cinnamaldehyde and epicatechin, in reducing the risk of developing Alzheimer’s Disease.
Authored by graduate student Roshni George, the paper suggests that these compounds could interfere with the pathological hyperphosphorylation of tau which leads to the aggregation of intracellular proteins, often termed ‘neurofibrillary tangles’ . This abnormal protein debris is a key marker of Alzheimer’s pathology, with extracellular amyloid plaques being another.
George et al demonstrated that applying the lipid, cinnamaldehyde in vitro inhibited filamentous tangles of tau proteins. They posit that this occurs because the oil binds cysteine residues on tau, reducing their instability and protecting them from oxidative stress. The group used a cysteine double mutant to show that the protective effect is mediated through these residues. This oxidative stress is the result of the formation of reactive oxygen species, including peroxides, during oxidative phosphorylation to produce glucose via the electron transport chain. The unstable molecules have the potential to react with lipids, proteins and DNA, changing their activity. To combat this, cells employ enzymes and polyphenol antioxidants to break down peroxides and sequester reactive free radicals. Epicatechin is one such antioxidant substance and it also interacts with the vulnerable cysteine residues of tau to inhibit its phosphorylation in vitro.
The neuroprotective role of these small molecules present in the spice present a novel avenue for research into preventative treatments for the degenerative disease, which affects almost half (45%) of Americans over 85s and one third of over 95s in the UK.