Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

Abstract

In recent years, neurological and neurodegenerative disorders research has focused on altered molecular mechanisms in search of potential pharmacological targets, e.g., imbalances in mechanisms of response to oxidative stress, inflammation, apoptosis, autophagy, proliferation, differentiation, migration, and neuronal plasticity, which occur in less common neurological and neurodegenerative pathologies (Huntington disease, multiple sclerosis, fetal alcohol spectrum disorders, and Down syndrome). Here, we assess the effects of different catechins (particularly of epigalocatechin-3-gallate, EGCG) on these disorders, as well as their use in attenuating age-related cognitive decline in healthy individuals. Antioxidant and free radical scavenging properties of EGCG -due to their phenolic hydroxyl groups-, as well as its immunomodulatory, neuritogenic, and autophagic characteristics, makes this catechin a promising tool against neuroinflammation and microglia activation, common in these pathologies. Although EGCG promotes the inhibition of protein aggregation in experimental Huntington disease studies and improves the clinical severity in multiple sclerosis in animal models, its efficacy in humans remains controversial. EGCG may normalize DYRK1A (involved in neural plasticity) overproduction in Down syndrome, improving behavioral and neural phenotypes. In neurological pathologies caused by environmental agents, such as FASD, EGCG enhances antioxidant defense and regulates placental angiogenesis and neurodevelopmental processes. As demonstrated in animal models, catechins attenuate age-related cognitive decline, which results in improvements in long-term outcomes and working memory, reduction of hippocampal neuroinflammation, and enhancement of neuronal plasticity; however, further studies are needed. Catechins are valuable compounds for treating and preventing certain neurodegenerative and neurological diseases of genetic and environmental origin. However, the use of different doses of green tea extracts and EGCG makes it difficult to reach consistent conclusions for different populations.

Phenolic Characterization and Neuroprotective Properties of Grape Pomace Extracts

“…Indeed, catechin, caftaric acid, and gallic acid were reported to be among the main phytochemicals present in both grape and pomace [ 21 , 22 , 23 , 24 ]. Intriguingly, catechins, besides having well known antioxidant activities [ 25 ], have been described as effective in treating and preventing different neurodegenerative and neurological disorders, although the heterogeneity of the studies reported in literature makes the drawing of reliable conclusions difficult [ 26 ]. Additionally, different studies suggest the capability of these compounds to cross the blood—brain barrier [ 27 , 28 , 29 ], which makes the evaluation of neuroprotective effects of extracts containing significant amounts of catechins sensible, as in the case of grape pomace.…”

Green Tea Catechins Modulate Skeletal Development with Effects Dependent on Dose, Time, and Structure in a down Syndrome Mouse Model

“…DYRK1A inhibitors such as epigallocatechin-3-gallate (EGCG) have been proposed for therapy in DS, because several studies have demonstrated an amelioration of brain, cognitive, and craniofacial deficits associated with DS [ 5 , 17 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. However, the effects of EGCG as a therapeutic agent for skeletal development are not consistent, with studies showing both positive and negative effects depending on the timing and dose of treatment [ 26 ]. The administration of pure EGCG (9 mg/kg/day) in 3-week-old mice had a rescuing effect on the femoral BMD and trabecular microarchitecture [ 6 ], whereas treatment with 20 mg/kg/day of EGCG starting at week 3 for 7 weeks showed no improvements in trabecular bone and limited improvements in cortical measurements [ 27 ].…”

Green Tea Intake and Parkinson's Disease Progression: A Mendelian Randomization Study

“…In addition, we also noticed an association with borderline significance between green tea intake and progression to HY-3 stage (OR = 0.94, 95 % CI: 0.89–1.00, P = 0.054), which described the overall motor symptom progression of PD. Green tea might exert this effect by modulating microglia activation and decreasing the production of inflammatory mediators ( 31 ). Similarly, a previous clinical study found that drinking green tea could improve antioxidant status and reduce oxidative damage ( 32 ), suggesting the potential beneficial role of green tea in the progression of PD.…”