Role of Blueberries in Neuronal Protection: New Perspectives on Alzheimer’s and Neurodegenerative Disease Prevention
Dementia is the loss of cognitive functions. Alzheimer’s disease (AD), the most common form of dementia, is a neurodegenerative disease that affects the structural integrity of the brain and accounts for 60-80% of dementia cases.
While the causes of AD are still unknown, several hypotheses have been proposed: deficits in cholinergic transmission, beta-amyloid (Aβ) plaques, tau tangles, oxidative damage and mitochondrial dysfunction, neuronal inflammation, synaptic loss, vascular changes, endosomal abnormalities, among others.
Genetics also play a role in AD, such as mutations in the genes for the epsilon 4 allele of apolipoprotein E (APOE-ε4), amyloid precursor protein (APP), and presenilin (PS1 and PS2).
Many of these hypotheses are interconnected and collectively lead to neuronal death. For example, cholinesterase (including acetylcholinesterase and butyrylcholinesterase) is a critical enzyme in regulating neurotransmitter levels and therefore plays an important role in cholinergic signaling.
Lifestyle changes, however, may hold the keys to AD prevention and potentially slowing the disease’s progression. Consuming foods rich in phenolic compounds like blueberries is part of a healthy lifestyle that can contribute to neuroprotection and help slow the decline in cognitive function.
Blueberries are rich in polyphenolic compounds and have been shown to improve cognitive function in several clinical studies.
However, the molecular basis of blueberries’ neuronal protection is not fully understood.
The aim of this research is to understand the biochemical basis of blueberries’ neuronal protection effects through their impact on various enzymes and pathways involved in Alzheimer’s disease (AD) and other neurodegenerative diseases.
The inhibitory effects of blueberries on the enzymatic activity of cholinesterase (acetylcholinesterase, AChE; and butyrylcholinesterase, BuChE), tyrosinase, and cyclooxygenase-2 (COX-2) have been examined.
The effects of blueberries on acetylcholinesterase biosynthesis in a cellular model have also been studied.
Furthermore, the effect of blueberries on amyloid fibril formation has been evaluated.
The results showed that blueberries directly inhibit the enzymatic activity of AChE, BuChE, tyrosinase, and COX-2, with an IC50 of 48 mg/mL, 9 mg/mL, 403 mg/mL, and 12 mg/mL equivalent to fresh berries, respectively.
Moreover, blueberries delay 24-hour amyloid fibril formation at 39 mg of fresh berry/mL.
They also reduce acetylcholinesterase synthesis at 19 mg of fresh berry/mL in a cellular model.
These results suggest that the neuroprotective effects of blueberries may involve different pathways, including enhancing cholinergic signaling through their effect on cholinesterase, reducing neurological inflammation through COX-2 inhibition, and reducing amyloid formation.
Ultimately, blueberries may play a vital role in neuronal protection in addition to their antioxidant activity, and the results provide further molecular mechanisms for their neuroprotective effects, supporting the idea of blueberries as nutraceuticals to enhance cognitive function.
If your company wishes to create or manufacture a product to improve cognitive function
