Alzheimer’s disease (AD) is the most common neurodegenerative disorder that affects the elderly. AD is characterized by a progressive impairment of memory and other cognitive skills leading to dementia. The major pathogenic factor associated to AD seems to be amyloid-beta peptide (Aβ) oligomers that tend to accumulate extracellularly as amyloid deposits and are associated with reactive microglia and astrocytes. The abnormal production by glia cells of pro-inflammatory cytokines, chemokines, as well as reactive oxygen and nitrogen species, can disrupt nerve terminals activity causing dysfunction and loss of synapses, which correlates with memory decline. These are phenomena preceding the neuronal death associated with late stages of AD. Therefore therapeutic strategies directed at controlling the activation of microglia and astrocytes and the excessive production of pro-inflammatory and pro-oxidant factors may be valuable to control neurodegeneration.
The researchers in this study investigated the protective effects of anthocyanins in a rat model against oxidative stress, neuroinflammation, induced memory impairment and neurodegeneration in rat hippocampus and cortex regions. In the rat model D-gal is used to induce oxidative stress to mimic natural aging. Rodents treated with D-gal have been commonly used as representative models for anti-aging research in the world.
The results indicated that anthocyanins treatment significantly improved behavioral performance of D-gal-treated rats in the so called Morris water maze and Y-maze tests. One of the potential mechanisms of this action was decreased expression of the receptor for advance glycation end product, reduced level of reactive oxygen species (ROS) and lipid peroxidation. The results also indicated that anthocyanins inhibited activated astrocytes and neuroinflammation via suppression of various inflammatory markers including p-NF-KB, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNF-α) in the hippocampus and cortex regions. Anthocyanins also stopped neuroapoptosis and improved deregulated synaptic proteins.
The rats in this study were intraperitoneally injected with anthocyanins once daily for 7 weeks. Therefore it is not possible to calculate dosing for human oral supplemetation. Research using oral supplemetation is therefore welcomed in order to estimate effective dosing values for humans.
Overall the test results in the rat model suggest that anthocyanins hold promise to be a safe anti-oxidant and anti-neuroinflammatory agent for age-related neurodegenerative diseases such as Alzheimer’s disease.
The study can be found here.