# The Role of Beetroot Ingredients in the Prevention of Alzheimer's Disease
## 2 General Characteristics of Alzheimer's Disease
### Individual Bioactive Compounds from Beetroots in the Prevention and Treatment of AD Nitric Pigments
In the group of animals receiving paracetamol and diclofenac as well as betanin supplementation (25 mg/kg b.w. ), the authors observed a lessening of oxidative stress and a reduction of most biochemical and histopathological changes due to the excessive consumption of paracetamol and diclofenac. The eventual conclusion was that betanin may serve as an effective neuroprotective agent. [PERSON] et al. [43] conducted a study in a group of mice intraperitoneally administered with trimethyltin chloride (single intraperitoneal injection of 2.6 mg/kg b.w.) to induce a neurodegenerative disorder. The therapeutic dose of betanin dissolved in normal saline was administered orally at 50 and 100 mg/kg b.w. The authors observed that when dosed at 100 mg/kg b.w., betanin showed neuroprotective activity against the neurodegenerative condition induced with trimethyltin chloride. [PERSON] et al. [44] studied the impact of betalin pigments present in beet plants on the process of \(\beta\)-amyloid aggregation, i.e., one of the causes of AD. The conducted analyses showed inhibition of \(\beta\)-amyloid aggregation, which confirmed that betalin pigments may provide an effective tool in the fight against AD. The hypotheses were corroborated with the use of the thioflavin T fluorescence test, circular dichroism spectroscopy, and electron microscopy observations (TEM). Thioflavin T is a fluorescent pigment that binds with \(\beta\)-amyloid. As a result, the fluorescence level is increased. The betalin pigments were used in a range of concentrations (6.25, 12.5, 25, and 50 uM). For each concentration, reduced fluorescence levels were observed, which suggests that the pigments inhibited the process of forming pathological \(\beta\)-amyloid structures. [PERSON] and [PERSON] [45] evaluated the protective activity of beetroot juice against neurotoxic aluminum in the brains of male rats (the toxic dose of 20 mg/kg b.w. of aluminum chloride was administered intraperitoneally, once daily, from the 14 th day of the experiment until its conclusion). The authors observed that administration of beetroot juice dosed at 15 mL/kg b.w. via a gastric tube, once daily over a period of 6 weeks, yielded positive effects in terms of protection against the oxidative stress induced by aluminum chloride. The level of GSH in the brain was increased after the application of the therapeutic juice dose, as compared to the group receiving only the toxic aluminum dose and was, respectively, 21.74 \(\pm\) 1.18 and 11.14 \(\pm\) 0.81 mg GSH/g of cerebral tissue. The activity of acetylcholinesterase increase (AchE) in the brain was reduced after administering the juice to 428.60 \(\pm\) 23.16 from 593.80 \(\pm\) 30.07 units AchE/g of cerebral tissue, relative to the group receiving only the toxic dose of aluminum. [PERSON] et al. [46] conducted a study on rats with a view to determining the protective potential of betanin against AD induced with aluminum chloride (administered orally, 100 mg/kg b.w.). Aluminum is a strong neurotoxin triggering oxidative stress, one of the causes of neurodegenerative diseases. The tested rats received oral doses of betanin (10 and 20 mg/kg b.w.) over a period of 4 weeks. Betanin was reported to have likely reduced learning disorders and caused tissue damage and cholinergic disfunction by inhibiting oxidation. Both of the betanin doses tested reduced the activity of acetylcholinesterase relative to the group receiving only the toxic dose of aluminum chloride. An increase in glutathione level was also observed relative to the group receiving aluminum chloride. The researchers concluded that betanin may be a promising bioactive compound in the pharmacotherapy of neurodegenerative diseases such as AD. [PERSON] et al. [47] studied the anti-inflammatory activity of betanin in simulated microglia cells in terms of the potential to reduce neuroinflammation.