Here is a list of twenty main anti-cognitive-impairment fruits and vegetables.
1. Berries on Brain Function:
The polyphenolic compounds contained in berries have been shown to cross the blood brain barrier and localize in various brain regions important for learning and memory. Talavera et al (2005) confirmed this in their research that showed increased total anthocyanin content in the brain on anthocyanin enriched diet (blackberry anthocyanins and peonidin 3-O-glucoside).
Plant polyphenols appear to have direct actions on signaling pathways involved in stress protection in neurons. This view further supports the potential for effective nutritional interventions to attenuate brain ageing, neuro-degeneration, and functional declines. Blueberry (Vactinium ashei) and blackberry (Rubus fruticosus/Rubus ulmifolius) contain anti-oxidant anthocyanins and thus are especially good for the brain. Blueberries have the highest anti-oxidant capacities among fruits and vegetables. Blueberries also reverse age-related declines in neuronal signal transduction as well as cognitive and motor deficits.
Supplementation with the blueberry extract concentrated in polyphenols to adult mice showed significant cognitive enhancement. The higher anti-oxidant potential inhibits AChE activity and increases hippocampal plasticity Lau et al. (2005 and 2007) and Casadesus et al. (2004). Higher intake of flavonoids, particularly from berries, appears to reduce rates of cognitive decline in older adults.
The measurement of anthocyanins and flavanols in the brain following blueberry supplementation may indicate that changes in spatial working memory in aged animals are linked to the effects of flavonoids on the extracellular signal-related kinase – cAMP-response element-binding protein – brain-derived neurotropic factor pathway.
The beneficial effects of blueberry extract, according to Brewer et al. (2010), may involve transient stress signaling and oxyradical production protection that may translate into improved cognition, reversed cognitive declines in object recognition and reduced number of neuro-degenerative processes in the brain of aged animals.
A non-significant trend was noted by Crews et al. (2005) on a subjective, self- report questionnaire where twice as many participants in the cranberry group rated their overall abilities to remember by treatment end as “improved” compared to placebo controls. Blueberry, cranberry, strawberry, and blackberry significantly attenuated age-related motor and cognitive deficits and reversed neuronal and behavioral (cognitive) function in aged rats.
Vepsäläinen et al (2013) found that anthocyanin-rich bilberry and blackcurrant diets also favorably modulated the processing of amyloid precursor protein and alleviated behavioral abnormalities in a mouse model of Alzheimer’s disease.
Ramirez et al. (2005) showed that lyophilised berries (blueberry, bilberry) significantly enhanced short-term memory, but not long-term memory in the inhibitory avoidance task, and induced an increase in the number of crossings in the first exposure to the open field. However, treated rats did not present any improvement of memory retention in open field habituation.
In contrast, Barros et al. (2006) showed that the administration of a lyophilized extract of blue berries significantly enhanced long-term memory in the inhibitory avoidance task, induced an increase in the number of crossings during open-field habituation and had an anxiolytic effect in the elevated plus-maze task. Moreover, the extract reduced oxidative DNA damage in brain tissue in vitro suggesting that supplementation with Vaccinium ashei berries to mice improves performance on memory tasks and has a protective effect on DNA damage, possibly due to the anti-oxidant activity of polyphenols, including anthocyanins.
However, Joseph et al. (1999) opined that anti-oxidant activity alone cannot predict the potency of these compounds against certain disorders affected by ageing suggesting that berry fruit polyphenols may possess a multiplicity of actions aside from anti-oxidant activity. Other possible mechanisms for the berry fruit’s positive effects include: direct effects on signaling to enhance neuronal communication, the ability to buffer against excess calcium, enhancement of neuro-protective stress shock proteins, and reduction of stress signals such as nuclear factor κ B (NF- κB).
2. Grape Seeds (Vitis Vinifera):
Sreemantulu et al. (2005) provided scientific support for the anti-stress (adaptogenic), anti-oxidant and no tropic activities of grape seed extract and substantiated the traditional claims for the usage of grapes and grape seeds in stress induced disorders. Intake of pro-anthocyanidin from grape seed extract in moderately low quantity was found to be effective in up-regulating the anti-oxidant defense mechanism by attenuating lipid peroxidation and protein oxidation.
Changes in the cholinergic system, however, indicated an increase in the acetyl choline concentration with a moderate reduction in acetylcholine esterase activity, suggesting that pro-anthocyanidin has a potent role in enhancing cognition in older rats. Balu et al. (2005; 2006) revealed that grape seed extract has inhibiting effect on the accumulation of age-related oxidative DNA damages in spinal cord and in various brain regions such as cerebral cortex, striatum and hippocampus.
Liu et al. (2011) and Wang et al. (2008) observed Grape seed polyphenolic extract to inhibit Aβ oligomerization in vitro and attenuate cognitive impairment and AD-related neuropathology in the brains of transgenic mice. Ashadevi et al. (2011) demonstrated it to be a neuro-protectant in the hippocampus and a preventive agent in cognitive loss with ageing.
3. Amla (Emblica Officinalis):
Amla churna, an Ayurvedic preparation, (50,100, and 200 mg/kg, p.o.) produced a dose-dependent improvement in memory scores of young and aged rats. Furthermore, it reversed the amnesia induced by scopolamine (0.4 mg/kg, i.p.) and diazepam (1 mg/kg, i.p.). The churna may prove to be a useful remedy for the management of Alzheimer’s disease on account of its multifarious beneficial effects such as, memory improving property, cholesterol lowering property and anti-cholinesterase activity and thus may be useful for the treatment of cognitive impairments induced by cholinergic dysfunction.
4. Litchi (Litchi Chinensis):
Oligomerised litchi fruit-derived polyphenol OLFP, also called Oligonol has been reported to attenuate early cognitive impairment in male senescence-accelerated mice, and diminish stress of the endoplasmic reticulum in neuronal cells.
5. Mulberry (Morus Nigra):
The berries being a rich source of Zea-xanthin, Lutein, Resveratrol – another polyphenol flavonoid, along with Iron, ß carotene, Vitamin K and B complex vitamins are potential natural cognitive enhancers and neuro-protectants. It was found that anthocyanin in mulberry fruit, could protect against cerebral ischemia. Kaewkaen et al. (2012) observed that mulberry fruit extract enhanced memory and the effect might be partly associated with the increased cholinergic function and its neuro-protective effect, and partly via the decreased oxidative stress in hippocampus.
6. Olives:
De Nicoló et al. (2013) showed that olive polyphenols may increase the levels of nerve growth factor and brain-derived neurotropic factor in crucial areas of the limbic system and olfactory bulbs. These factors play a key role in learning and memory processes, and in the proliferation and migration of endogenous progenitor cells present in the rodent brain.
7. Mango (Mangifera Indica):
Chronic treatment (7 days) of the ethanolic extract of Mangifera indica fruit and vitamin C significantly (p < 0.05) reversed the ageing and scopolamine induced memory deficits as judged by the step down passive avoidance task and elevated plus-maze task in mice.
8. Soya (Glycine Max):
Kritz-Silverstein et al. (2003) reported that soya isoflavone supplementation has a favorable effect on cognitive function, particularly verbal memory, in postmenopausal women. Thorp et al. (2009) found soya isoflavone supplementation in healthy males enhanced cognitive processes which appear to be dependent on oestrogen activation.
Although data from humans, cultures, and animal models show soy isoflavones to have a positive effect on brain function, Lee et al. (2005) who found it to be difficult to elucidate the mechanism of action on cognitive function and the nervous system, suggested two putative pathways – (1) an estrogen receptor-mediated pathway and (2) inhibition of tyrosine kinase, in particular by genistein. Soya derived phosphatidylserine has been shown to have beneficial effects on cognitive functions. Phosphatidylserine containing omega-3 fatty acids significantly improved immediate verbal recall in the treatment group compared to the placebo group and cognitive performance in non-demented elderly with memory complaints.
The investigation by Ding et al. (2011, 2013a) showed that soya isoflavone reduced the cytokine cascade and inflammatory response induced by Aβ1-42 which could result in the improvement of spatial learning and memory in the rats. Its mechanism might be associated with the protection of synaptic plasticity by improving the synaptic structure and regulating the synaptic related proteins. Soya isoflavone could alleviate the oxidative damage and maintain the redox imbalance in brain mitochondria damaged by Aβ1-42. This might result from regulation of the Nrf2/HO-1 pathway.
9. Saffron (Crocus Sativus):
Saffron’s active constituent is crocin (crocetin di-gentiobiose ester). Ghadrdoost et al. (2011) found crocin significantly decreased plasma levels of corticosterone, as measured after the end of stress. Their observations indicate that saffron and its active constituent crocin can prevent the impairment of learning and memory as well as the oxidative stress damage to the hippocampus induced by chronic stress thus, proving that saffron may be useful in pharmacological alleviation of cognitive deficits.
Abe and Saito (2000) found saffron extract to improve ethanol-induced impairments of learning behaviors, prevent hippocampal long-term potentiation, and a form of activity-dependent synaptic plasticity that may underlay learning and memory. This effect of saffron extract is attributed to crocin but not crocetin. Crocin and daunorubicin inhibits neuronal cell death induced by both internal and external apoptotic stimuli.
10. Cumin Seeds (Cuminum Cyminum):
Koppula and Choi, (2011) found the cognition, as determined by the acquisition, retention, and recovery in rats, to be dose-dependent and provided scientific support for the anti-stress, anti-oxidant, and memory-enhancing activities of cumin extract. They also substantiated that the traditional use of cumin seeds as a culinary spice in foods is beneficial.
11. Black Cumin Seeds (Nigella Sativa):
Experimental evidences have demonstrated that Nigella sativa seed (NS) has positive modulation effects on aged rats with memory impairments. These seeds prevent hippocampal pyramidal cell loss and enhance consolidation of recall capability of stored information and spatial memory in rats. Bin Sayeed et al. (2013) demonstrated the role of NS in enhancing memory, attention and cognition. Therefore, further investigations are needed on black cumin seed as a potential food supplement for preventing or delaying the progress of Alzheimer disease.
12. Noni (Morinda Citrifolia):
Noni is widely used for different illnesses including disorders of central nervous system. Recently, Noni has been reported to prevent amyloid beta induced memory impairment in mice. Ethanolic extract of Noni fruits and its chloroform and ethyl acetate fractions significantly improved memory and cerebral blood flow. However, butanol fraction had no effect. Further, increased oxidative stress and AChE activity following scopolamine was significantly attenuated in a dose dependent inhibition in vitro by ethanolic extract of Noni and its fractions.
13. Wolf Berries (Lycium Barbarum):
It has been shown that pre-treatment using extracts of Lycium barbarum containing mostly polysaccharides (LBP) could protect the cultured primary cortical neurons from β-amyloid peptide neurotoxicity. Yang et al. (2012) showed a seven-day oral pre-treatment with LBP, to effectively improve neurological deficits, decrease infarct size and cerebral edema as well as protect the brain from blood brain barrier disruption, aquaporin-4 up-regulation, and glial activation.
LBP may be used as a prophylactic neuro-protectant in patients at high risk for ischemic stroke. Ho et al. (2010) also demonstrated that LBP exerted neuro-protective effects on cortical neurons exposed to plasma homocystine and thus has the potential to be a disease modifying agent for the prevention of AD.
14. Brahmi (Bacopa Monnieri):
An Australian survey showed brahmi to be one of the most popular aids for memory among 60-64-year- old consumers. Laboratory studies on rats indicate that extracts of the plant improve memory capacity. Some studies in mice suggest that ingestion of Bacopa for a 12 week period can significantly improve cognitive ability by accelerating the rate of learning and enhancing memory. Memory-enhancing effects of brahmi have been attributed to saponins (bacosides, bacopasides, or bacopasaponins). Bacopasaponin constituents have been shown to facilitate mental retention in avoidance response in rats.
Bacopasaponin have also been shown to reverse amnesic effects of neurotoxin, scopolamine, phenytoin, electroshock, and immobilization stress and diazepam-induced amnesia in the Morris water maze test.
In some trials, though the extract did not restore or enhance memory formation, it did improve retention. Aged human subjects treated with standardized brahmi extract of 300 mg/day orally for 12 weeks confirmed it as a potential and safe cognitive performance enhancer. In 98 healthy older people over 55 years of age Bacopa significantly improved memory acquisition and retention. A recent systematic review found some evidence to suggest that Bacopa improves memory free recall, but there was a lack of evidence for enhancement of other cognitive abilities.
Treatment with brahmi reduced beta-amyloid levels in the brain of an Alzheimer’s disease doubly transgenic mouse model of rapid amyloid deposition (PSAPP mice) suggesting brahmi to be therapeutically useful for the treatment of cognitive impairment, thus supporting its possible anti-Alzheimer’s properties.
Apart from these, co-administration of Bacopa extract during aluminium treatment significantly prevented the aluminium-induced decrease in SOD activity as well as the increased oxidative damage to lipids and proteins. Protective effect was also observed at microscopic level.
These observations showed that Bacopa’s neuroprotective effects were comparable to those of l-deprenyl at both biochemical and microscopic levels. Several observations have strongly implicated that Bacopa monniera has potential to protect brain from oxidative damage resulting from aluminum toxicity and MeHg-induced neurotoxicity in rat.
15. Mandukaparni (Centella Asiatica):
Centella asiatica (CA) is a common medicinal plant used in the ayurvedic system of medicine to treat various ailments and as a memory enhancer. Ashwagandha, Brahmi, Vacha, and Shank Pushpi at the right proportions are found to work in combination to prevent mental restlessness and agitation.
The Medhya rasayana are a group of medicines in Ayurveda known to act on the nervous system have been claimed to improve mental ability. These drugs contain mainly extracts from plants such as Centella asiatica, Acorus calamus, jatamansi and Bacopa monnieri. Brahmi is a great herb for the brain. But without Ashwagandha, Brahmi has a different effect and is not as helpful.
CA grows in wet places throughout India. It is used in ayurvedic preparations either as whole plants or as leaves in the fresh or extract form. It is also used as a tonic for promoting brain growth and improving memory. In addition, the plant is used in children with learning difficulties to improve general mental ability and in people suffering from cognitive disorders. Fresh leaf juice (extract) of CA has been claimed to improve learning and memory in different clinical studies.
Administration of fresh leaf extracts of CA during the growth spurt (neonatal) period facilitates dendritic growth in the hippocampal CA3 neurons. Increased dendritic arborization may be the neuronal basis, for the improved learning and memory reported earlier.
Brahmi rasayana (BR) significantly improved learning and memory in young mice and reversed the amnesia induced by both scopolamine (0.4 mg kg(-1) i.p.) and natural ageing. BR significantly decreased whole brain acetyl cholinesterase activity. BR might prove to be a useful memory restorative agent in the treatment of dementia seen in elderly.
Shinomol and Muralidhara (2008 a) observed that CA has the propensity to modulate both endogenous and neuro-toxicant induced oxidative impairments in the brain and may be effectively employed as a neuro-protective adjuvant to abrogate oxidative stress in vivo, and opined that it may be wholly or in part related to the enhancement of glutathione, thiols and antioxidant machinery in the brain regions of prepubertal mice.
Dhanasekaran et al (2009) reported that CA can impact the amyloid cascade altering amyloid beta pathology in the brains of PSAPP mice and modulating components of the oxidative stress response that has been implicated in the neuro-degenerative changes in Alzheimer’s disease.
16. Okra (Abelmoschus Esculentus):
Quercetin, rutin and okra extract treatments reversed cognitive deficits, including impaired dentate gyrus cell proliferation, and protected against morphological changes in the CA3 region in dexamethasone-treated mice.
17. Buck Wheat (Fagopyrum Esculentum):
Pu et al (2004) observed that Buckwheat polyphenol (BWP) ameliorate spatial memory impairment by inhibiting glutamate release and the delayed generation of NO(x)(-) in rats subjected to repeated cerebral ischemia.
18. Kokum (Garcinia Indica):
Garcinol, a naturally occurring Histone acetyl-transferase inhibitor derived from the rind of Kokum fruit regulates chromatin function and hence useful in the treatment of newly acquired or recently reactivated traumatic memories.
19. Wheat Germ:
Wheat germ is a powerful brain food because it is rich in vitamin E and selenium (both very potent anti-oxidant nutrients), as well as choline and magnesium.
The development of biotech drugs such as peptides and proteins that act in the central nervous system has been significantly impeded by the difficulty of delivering them across the blood-brain barrier. Improvements in spatial memory in ethyl choline aziridium-treated rats were observed following intranasal administration of 25 micro g/kg and 12.5 micro g/kg of vasoactive intestinal peptide loaded by unmodified nano-particles and wheat germ-agglutinin-modified nano-particles, respectively.
Distribution profiles of wheat germ agglutinin-conjugated nanoparticles in the nasal cavity presented their higher affinity to the olfactory mucosa than to the respiratory mucosa. Inhibition experiment with specific sugars suggested that the interaction between the nasal mucosa and the wheat germ agglutinin-functionalized nanoparticles were due to the immobilization of carbohydrate-binding pockets on the surface of the nano-particles. The results clearly indicated wheat germ agglutinin- modified nano-particles might serve as promising carriers especially for biotech drugs such as peptides and proteins.
20. Coffee:
The larger improvement of performance in fatigued subjects confirms that caffeine is a mild stimulant. Caffeine has also been reported to prevent cognitive decline in healthy subjects but the results of the studies are heterogeneous, some finding no age- related effect while others reported effects only in one sex and mainly in the oldest population. In conclusion, it appears that caffeine cannot be considered a pure cognitive enhancer.
Its indirect action on arousal, mood and concentration contributes in large part to its cognitive enhancing properties. The cognitive and mood effects of caffeine are well documented. Caffeine, in a dose-dependent manner, mitigated many adverse effects of exposure to multiple stressors. Caffeine (200 and 300 mg) significantly improved visual vigilance, choice reaction time, repeated acquisition, self-reported fatigue and sleepiness with the greatest effects on tests of vigilance, reaction time, and alertness. Even in the most adverse circumstances, moderate doses of caffeine can improve cognitive function, including vigilance, learning, memory, and mood state.
Besides improving cognitive function, chronic coffee consumption modulated the endogenous anti-oxidant system in the brain. Therefore, chronic coffee ingestion, through the protection of the anti-oxidant system, may play an important role in preventing age-associated decline in the cognitive function. Caffeine intake was found to be related to moderately better cognitive maintenance over 5 years in older women with vascular disorders.
Aged rats supplemented with a 0.55 per cent coffee diet, equivalent to ten cups of coffee, performed better in psychomotor testing (rotarod) and in a working memory task (Morris water maze) compared to aged rats fed a control diet. A diet with 0.55 per cent coffee appeared to be optimal. The 0.165 per cent coffee-supplemented group (three cups) showed some improvement in reference memory performance in the Morris water maze.
In a subsequent study, the effects of caffeine alone did not account for the performance improvements, showing that the neuro-protective benefits of coffee are not due to caffeine alone, but rather to other bioactive compounds in coffee. The findings of Jang et al. (2013) also suggested that caffeine-free decaffeinated coffee may prevent memory impairment in human through the inhibition of NF- κB activation and subsequent TNF-α production.
Smith (2013) observed that caffeine interacted with extraversion in the predicted direction for serial recall and running memory tasks. Caffeine improved simple reaction time and the speed of encoding of new information, effects which were not modified by extraversion thus implying possible biological mechanisms underlying effects of caffeine on cognitive performance.