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Cited by 29Medicinal Plants and NeuroprotectionAlzheimer's disease research and treatmentsCholinesterase and Neurodegenerative Diseases

The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment

Open access
Zieneldien, Tarek, Kim, Janice, Cao, Chuanhai·2022·Geriatrics
DOI 10.3390/geriatrics7020024PMC PMC8938774
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Abstract

Alzheimer’s disease (AD) is an age-related, progressive neurodegenerative disorder characterized by impaired cognition, memory loss, and altered personality. Many of the available pharmaceutical treatments do not alter the onset of disease progression. Recently, alternatives to developed drug candidates have been explored including medicinal plants and herbal treatments for the treatment of AD. This article examines the role of herbal plant extracts and the neuroprotective effects as alternative modes of intervention for AD progression. These extracts contain key metabolites that culminate alterations in AD progression. The traditional plant extracts explored in this article induce a variety of beneficial properties, including antioxidants, anti-inflammatory, and enhanced cognition, while also inducing activity on AD drug targets such as Aβ degradation. While these neuroprotective aspects for AD are relatively recent, there is great potential in the drug discovery aspect of these plant extracts for future use in AD treatment.

AI snapshot

Written from the paper’s full text.

TL;DR

This narrative review summarizes preclinical and clinical evidence that medicinal plant extracts may slow or ameliorate Alzheimer’s disease (AD) through antioxidant, anti-inflammatory, anti-amyloid/tau, and cholinergic mechanisms. Several human trials report cognitive or mood benefits for extracts such as *Withania somnifera*, *Bacopa monnieri*, *Centella asiatica*, and *Crocus sativus*, but the authors note limited clinical data, bioavailability barriers, and the need for further research.

Key findings

  • AD is described as affecting more than 6 million individuals in the United States and approximately 50 million worldwide; genetic factors account for 5–10% of familial AD and 90–95% is sporadic, while age is the most critical risk factor, with about 3% affected at ages 65–74 and 17% at ages 75–84.
  • The review reports that only five drugs—galantamine, rivastigmine, donepezil, memantine, and donepezil plus memantine—were previously FDA-approved for AD, with aducanumab later receiving accelerated approval.
  • Selected herbal extracts are said to act on AD targets including Aβ degradation/clearance, tau hyperphosphorylation, cholinergic neurotransmission, oxidative stress, and neuroinflammation. Specific clinical examples include: *W. somnifera* 300 mg twice daily for 8 weeks in 50 subjects with mild cognitive impairment improved information-processing speed, attention span, and executive function; *B. monnieri* 125 mg twice daily for 12 weeks in 35 subjects aged 55+ improved paired-association learning, mental control, and logical memory at 8 and 12 weeks; *C. asiatica* at the highest dose (750 mg twice daily for 2 months) enhanced working memory and self-rated mood in 28 healthy subjects; saffron 30 mg/day improved ADAS-cog versus placebo over 16 weeks in 46 subjects with mild-to-moderate AD and was comparable to donepezil 10 mg/day over 22 weeks in 54 subjects and to memantine 20 mg/day over 12 months in 68 subjects with moderate-to-severe AD.
  • Curcumin from *Curcuma longa* reduced plaque loads, inflammation, amyloid pathology, and oxidative damage in animal models and improved cognition, but the review states that clinical studies of curcumin remain limited and its poor bioavailability, rapid metabolism, and limited blood–brain barrier penetration constrain translation.

Methods

  • Design: narrative review of herbal plant extracts and neuroprotective strategies for AD, covering proposed pathological mechanisms, selected plant extracts, and future delivery approaches.
  • Data/sample: the paper synthesizes cited in vitro, animal-model, and human clinical studies of plants including *Withania somnifera*, *Bacopa monnieri*, *Ginkgo biloba*, *Centella asiatica*, *Crocus sativus*, *Curcuma longa*, and Fuzhisan, as well as limited-study plants and cannabinoids.
  • Main analysis: qualitative synthesis of mechanisms and outcomes; no systematic search strategy, inclusion criteria, meta-analysis, or quantitative pooling is described in the provided text.

Limitations

  • The paper states that clinical data for *W. somnifera* in cognitive impairment are limited, that clinical studies using curcumin are limited in number, and that many other medicinal plants have mostly in vitro, in vivo, or observational data.
  • The paper states that curcumin has inefficient blood–brain barrier penetration, nominal bioavailability, rapid gastrointestinal metabolism, and chemical instability, and that intranasal delivery has limitations including small administration volume, limited olfactory epithelial surface area, and short retention time.
  • Evident from the text: as a narrative review, it does not report a systematic search, study-quality appraisal, or risk-of-bias assessment, so the summarized findings rely on heterogeneous cited studies and should be interpreted accordingly.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.3390/geriatrics7020024

Cites

208 of 208 references verified0 citation errors · 0 not checkable

Statistics

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Claims the paper makes

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  • Premisecitation

    Various molecular targets have been recognized as mediating pathophysiological processes.

    “As of now, various molecular targets have been recognized as mediating pathophysiological processes [35].”
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  • Premisecitation

    Cholinergic neuronal dysfunction in the brain could substantially contribute to Alzheimer's disease-related cognitive decline.

    “As such, the cholinergic hypothesis proposes that cholinergic neuronal dysfunction in the brain could substantially contribute to the AD-related cognitive decline [25].”
    Quote in the paperSubstantial claim0 of 1 sources checked
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  • Premisecitation

    Reducing the amount of amyloid-beta has been a major target in the development of Alzheimer's disease therapeutics.

    “As such, reducing the amount of Aβ has been a major target in the development of AD therapeutics [30,31,32].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [30] Izzo, N.J., Staniszewski, A., To, L., Fa, M., Teich, A.F., Saeed, F., Wostein, H., Walko, T., Vaswani, A., and Wardius, M. (2014). Alzheimer’s therapeutics targeting amyloid beta 1-42 oligomers I: Abeta 42 oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits. PLoS ONE, 9. source

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  • Premisecitation

    Only five drugs-galantamine, rivastigmine, donepezil, memantine, and a combination of donepezil and memantine-were previously FDA-approved for Alzheimer's disease treatment.

    “As such, despite the high prevalence of AD, only five drugs, consisting of galantamine, rivastigmine, donepezil, memantine, and a combination of donepezil and memantine, have been previously FDA-approved for its treatment [10].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] Tan, 2014, Efficacy and safety of donepezil, galantamine, rivastigmine, and memantine for the treatment of Alzheimer’s disease: A systematic review and meta-analysis, J. Alzheimer’s Dis. source

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  • Premisecitation

    The primary pathological causative factor of Alzheimer's disease is amyloid-beta accumulation.

    “Currently, there is a vast amount of evidence suggesting that the primary pathological causative factor of AD is Aβ accumulation [29].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [29] Hardy, 2002, The amyloid hypothesis of Alzheimer’s disease: Progress and problems on the road to therapeutics, Science source

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    Premisecitation

    Alzheimer's disease is perpetually accompanied by elevated oxidative cellular stress in the brain, yielded by elevated production of free radicals, reduced polyunsaturated fatty acid, elevated protein and DNA oxidation, elevated lipid peroxidation, and aggregation and accumulation of amyloid-beta.

    “In fact, a vast amount of evidence indicates that AD is perpetually accompanied by elevated oxidative cellular stress in the brain, yielded by the elevated production of free radicals, reduced polyunsaturated fatty acid, elevated protein and DNA oxidation, elevated lipid peroxidation, and the aggregation and accumulation of Aβ, which cause oxidative stress [28].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [28] Markesbery, 1997, Oxidative stress hypothesis in Alzheimer’s disease, Free Radic. Biol. Med. source

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    Premisecitation

    Neurofibrillary tangles are an Alzheimer's disease hallmark and principally consist of tau, a microtubule-associated scaffold protein.

    “Neurofribrillary tangles are also considered an AD hallmark and principally consist of tau, which is a microtubule-associated scaffold protein [22].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [22] Busche, 2019, Tau impairs neural circuits, dominating amyloid-β effects, in Alzheimer models in vivo, Nat. Neurosci. source

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    Premisecitation

    Bioactive components of traditional herbs provide neuroprotection and improved memory through their mechanisms of action.

    “These components provide neuroprotection and improved memory through their mechanisms of action [17].”
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    • cites [17] Eckert, 2010, Traditional used Plants against Cognitive Decline and Alzheimer Disease, Front. Pharmacol. source

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    Premisecitation

    Current pharmaceutical treatments for Alzheimer's disease mainly address symptoms and have limited effectiveness once the disease progresses in severity.

    “Scientific efforts to discover a cure for AD have been expensive and disappointing, with current drugs mainly addressing the symptoms of the disorder and having limited effectiveness once the disease progresses in severity [8,9].”
    • Also stated in: § Abstract · plain
      “Many of the available pharmaceutical treatments do not alter the onset of disease progression.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [8] Reitz, 2016, Toward precision medicine in Alzheimer’s disease, Ann. Transl. Med. source

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    • cites [9] Oxford, 2020, Clinical Trials in Alzheimer’s Disease: A Hurdle in the Path of Remedy, Int. J. Alzheimer’s Dis.

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    Premisecitation

    The pathological hallmarks of Alzheimer's disease are neurofibrillary tangles and neuritic plaques, associated with hyperphosphorylation of tau and accumulation of amyloid-beta in the brain.

    “Furthermore, the pathological hallmarks of AD consist of neurofibrillary tangles and neuritic plaques, which are associated with cytoskeletal changes attributed to the hyperphosphorylation of microtubule-associated tau and the accumulation of Amyloid-beta in the brain [14].”
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    • cites [14] Radanovic, 2012, Alzheimer’s disease, Subcell. Biochem. source

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    Premisecitation

    Continuous activation of brain immune cells such as microglia leads to release and production of proinflammatory cytokines, which aids tau and amyloid-beta pathologies and leads to loss of neurons.

    “Continuous activation of the brain’s immune cells, such as microglia, leads to the release and production of various proinflammatory cytokines, which aids tau and Aβ pathologies and leads to the loss of neurons [24].”
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    • cites [24] Kinney, 2018, Inflammation as a central mechanism in Alzheimer’s disease, Alzheimer’s Dement. source

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    Premisecitation

    The most prevalent hypotheses for Alzheimer's disease are the amyloid-beta cascade hypothesis, the inflammation hypothesis, the cholinergic hypothesis, the tau hypothesis, and the oxidative hypothesis.

    “The most prevalent hypotheses are the Aβ cascade hypothesis, the inflammation hypothesis, the cholinergic hypothesis, the tau hypothesis, and the oxidative hypothesis [18,19,20].”
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    • cites [18] Ricciarelli, 2017, The Amyloid Cascade Hypothesis in Alzheimer’s Disease: It’s Time to Change Our Mind, Curr. Neuropharmacol. source

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    • cites [19] Maccioni, 2010, The revitalized tau hypothesis on Alzheimer’s disease, Arch. Med. Res. source

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    • cites [20] Liu, 2019, History and progress of hypotheses and clinical trials for Alzheimer’s disease, Signal Transduct. Target. Ther. source

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    Interpretationnone given

    Natural products are advantageous because some exhibit neuroprotective effects through a plethora of differing approaches.

    “In general, natural products are advantageous because some have the ability to exhibit their neuroprotective effects through a plethora of differing approaches.”
    Quote in the paperSubstantial claim

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    Premisecitation

    The amyloid-beta cascade hypothesis implicates amyloid-beta peptides as the Alzheimer's disease causative agent due to extracellular deposition as senile plaques, with neurofibrillary tangles resulting in neuronal loss, dementia, and vascular damage.

    “The Aβ cascade hypothesis implicates Aβ peptides as the AD causative agent due to the extracellular deposition of the Aβ peptides as senile plaques, with the neurofibrillary tangles resulting in neuronal loss, dementia, and vascular damage [21].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [21] Hardy, 1992, Alzheimer’s disease: The amyloid cascade hypothesis, Science source

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    Premisecitation

    Popular neuroprotective strategies for Alzheimer's disease management include discovering small molecules that block amyloid-beta interactions with intracellular and extracellular targets to avoid caspase activation and proapoptotic protein expression, reduce stress kinase signaling cascades, inhibit tau protein phosphorylation, counterbalance cholinergic functional loss, and boost neuronalplastic

    “Popular neuroprotective strategies for AD management consist of discovering small molecules with the ability to block these Aβ interactions with intracellular and extracellular targets to avoid caspase activation and the expression of proapoptotic proteins, to reduce the stress kinase signaling cascades, to inhibit tau protein phosphorylation, to counterpoise cholinergic functional loss, and to bo”
    Quote in the paperNot a substantial claim0 of 5 sources checked
    • cites [37] Heneka, 2015, Neuroinflammation in Alzheimer’s disease, Lancet Neurol. source

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    • cites [38] Guimaraes, 2016, Alzheimer’s disease: Targeting the Cholinergic System, Curr. Neuropharmacol. source

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    • cites [39] Ding, 2019, Amyloid Beta Oligomers Target to Extracellular and Intracellular Neuronal Synaptic Proteins in Alzheimer’s Disease, Front. Neurol. source

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    • cites [40] Ferrera, 2011, Caspase-12 activation is involved in amyloid-β protein-induced synaptic toxicity, J. Alzheimer’s Dis. source

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    • cites [41] Iqbal, 2010, Tau in Alzheimer disease and related tauopathies, Curr. Alzheimer Res. source

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    Premisecitation

    Bacopa monnieri elicits its role via reduction in divalent metals, reduction in lipid peroxide formation, inhibition of lipoxygenase, and scavenging activity of reactive oxygen species.

    “B. monnieri elicits its role via the reduction in divalent metals, reduction in lipid peroxide formation, inhibition of lipoxygenase, and through its scavenging activity of reactive oxygen species [102].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [102] Dhanasekaran, 2007, Neuroprotective mechanisms of ayurvedic antidementia botanical Bacopa monniera, Phytother. Res. source

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    Premisecitation

    Withania somnifera treatment could mitigate Abeta toxicity while boosting longevity in Drosophila melanogaster models of Alzheimer's disease.

    “Consequently, Drosophila melanogaster models of AD have also elucidated that W. somnifera treatment could mitigate Abeta toxicity while seemingly boosting longevity [92].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [92] Halim, M.A., Rosli, I.M., Jaafar, S.S.M., Ooi, H.-M., Long, P.-W., Shamsuddin, S., Najimudin, N., and Azzam, G. (2020). Withania somnifera Showed Neuroprotective Effect and Increase Longevity in Drosophila Alzheimer’s Disease Model, Cold Spring Harbor Laboratory. source

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    Premisecitation

    Root extract treatments led to low-density lipoprotein receptor-related protein upregulation, thereby boosting amyloid-beta clearance and ameliorating Alzheimer's disease pathology in APP/PS1 mice.

    “Consequently, root extract treatments led to low-density lipoprotein receptor-related protein upregulation, thereby boosting Aβ clearance and ameliorating AD pathology in APP/PS1 mice [91].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [91] Sehgal, 2012, Withania somnifera reverses Alzheimer’s disease pathology by enhancing low-density lipoprotein receptor-related protein in liver, Proc. Natl. Acad. Sci. USA source

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    Premisecitation

    Bacopa monnieri is a nootropic herb with low toxicity and has been traditionally utilized as a memory booster and neural tonic.

    “B. monnieri is a nootropic herb with low toxicity and has been traditionally utilized as a memory booster and neural tonic in a plethora of ailments [95].”
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    • cites [95] Aguiar, 2013, Neuropharmacological review of the nootropic herb Bacopa monnieri, Rejuvenation Res. source

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    Interpretationcitation

    The synergistic action of herbal extracts and mixtures has the potential to eliminate severe adverse effects correlated with the utilization of a single xenobiotic product, allowing for a broader spectrum of activity and reducing the chances of pathogenic resistance.

    “Additionally, the synergistic action of herbal extracts and mixtures also has the potential to eliminate severe adverse effects correlated with the utilization of a single xenobiotic product, allowing for a broader spectrum of activity and reducing the chances of pathogenic resistance [43].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [43] Olila, 2001, Antibacterial and antifungal activities of extracts of Zanthoxylum chalybeum and Warburgia ugandensis, Ugandan medicinal plants, Afr. Health Sci.

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    Premisecitation

    Bacopa monnieri extract appeared to enhance escape latency time in the Morris water maze and blocked the diminishment of cholinergic neuron density in rat models.

    “In this case, the B. monnieri extract appeared to enhance the escape latency time in the Morris water maze and blocked the diminishment of cholinergic neuron density [56].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [56] Uabundit, 2010, Cognitive enhancement and neuroprotective effects of Bacopa monnieri in Alzheimer’s disease model, J. Ethnopharmacol. source

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    Premisecitation

    Treatment with withanolide A displays significant regenerative properties of dendrites and axons, and restorative properties of pre- and postsynapses in cultured neurons.

    “Consequent therapeutic treatment with withanolide A displayed significant regenerative properties of dendrites and axons, and even displayed restorative properties of the pre- and postsynapses in the cultured neurons [88].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [88] Tohda, 2000, Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells, Neuroreport source

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    Premisecitation

    Withania somnifera, as an adaptogen, possesses free radical scavenging, antioxidant, and immune-boosting activities.

    “W. somnifera, as an adaptogen, has been demonstrated to possess free radical scavenging and antioxidant and immune-boosting activities [78].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [78] Singh, 2011, An overview on ashwagandha: A Rasayana (rejuvenator) of Ayurveda, Afr. J. Tradit. Complement. Altern. Med. source

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    Premisecitation

    Withanolide A inhibits Abeta25-35-induced axonal and dendritic degeneration in the hippocampus and cerebral cortex, while also restoring synapses and amyloid-beta-peptide-induced memory impairment in mice.

    “Withanolide A has been shown to inhibit Abeta25-35-induced axonal and dendritic degeneration in the hippocampus and cerebral cortex, while also seemingly restoring synapses and Aβ -peptide-induced memory impairment in mice [89].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [89] Kuboyama, 2005, Neuritic regeneration and synaptic reconstruction induced by withanolide A, Br. J. Pharmacol. source

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    Premisecitation

    Administering semipurified extracts of Withania somnifera orally inhibited amyloid-beta peptide accumulation and reversed behavioral impairment in APP/PS1 mice models of Alzheimer's disease.

    “Similarly, administering semipurified extracts of W. somnifera orally inhibited Aβ peptide accumulation and reversed behavioral impairment in APP/PS1 mice models of AD [91].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [91] Sehgal, 2012, Withania somnifera reverses Alzheimer’s disease pathology by enhancing low-density lipoprotein receptor-related protein in liver, Proc. Natl. Acad. Sci. USA source

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    Premisecitation

    Withanamides A and C bind to the active motif of Abeta-25-35 and avert the formation of fibrils.

    “Molecular modeling research studies have elucidated that withanamides A and C have the ability to bind to the active motif of Abeta-25-35 and avert the formation of fibrils [85].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [85] Kumar, 2012, An aqueous extract of Withania somnifera root inhibits amyloid β fibril formation in vitro, Phytother. Res. source

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    Interpretationcitation

    Bacopa monnieri alone exhibited enhanced effects after continuous treatment, proposing repetitive dosing of Bacopa monnieri as a potential therapeutic alternative for subjects with mild cognitive impairment.

    “Likewise, B. monnieri alone exhibited enhanced effects after continuous treatment, proposing repetitive dosing of B. monnieri as a potential therapeutic alternative for subjects with MCI.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [106] Dimpel, 2016, Psychophysiological Effects of Sideritis and Bacopa Extract and Three Combinations Thereof—A Quantitative EEG Study in Subjects Suffering from Mild Cognitive Impairment (MCI), Adv. Alzheimer’s Dis.

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    Premisecitation

    Centella asiatica derivatives madasiatic acid, madecassoside, asiatic acid, and asiaticosides block hydrogen peroxide and beta-amyloid-induced cellular death and reduce the concentration of free radicals.

    “In vitro research studies utilizing madasiatic acid, madecassoside, asiatic acid, and asiaticosides C. asiatica derivatives have elucidated that these compounds have the ability to block hydrogen peroxide and beta-amyloid-induced cellular death, as well as to reduce the concentration of free radicals, thereby proposing a possible role for C. asiatica in AD treatment and prevention [64,132,133].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [64] Gupta, 2003, Effect of Centella asiatica on cognition and oxidative stress in an intracerebroventricular streptozotocin model of Alzheimer’s disease in rats, Clin. Exp. Pharmacol. Physiol. source

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    • cites [132] Xu, 2008, Gotu Kola (Centella Asiatica) extract enhances phosphorylation of cyclic AMP response element binding protein in neuroblastoma cells expressing amyloid beta peptide, J. Alzheimer’s Dis. source

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    • cites [133] Viegas, 2011, The role of natural products in the discovery of new drug candidates for the treatment of neurodegenerative disorders II: Alzheimer’s disease, CNS Neurol. Disord. Drug Targets source

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    Interpretationcitation

    Centella asiatica could be helpful in mitigating age-associated cognitive impairment while also boosting mood in healthy geriatric subjects.

    “The experimental results elucidate that the highest dosage indeed enhanced working memory, and improvements in self-rated mood were also noted post-treatment, implying that C. asiatica could be helpful in mitigating age-associated cognitive impairment while also boosting mood in healthy geriatric subjects [136].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [136] Wattanathorn, 2008, Positive modulation of cognition and mood in the healthy elderly volunteer following the administration of Centella asiatica, J. Ethnopharmacol. source

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    Premisecitation

    In Alzheimer's disease and vascular dementia subgroups, standard mean differences in the Syndrome Kurztest favored Ginkgo biloba over placebo, with 240 mg daily dosages having significantly enhanced standard mean differences.

    “In the AD and vascular dementia subgroups, the standard mean differences in the Syndrome Kurztest favored G. biloba over placebo treatment, with 240 mg daily dosages having significantly enhanced standard mean differences in the Syndrome Kurztest [128].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [128] Hashiguchi, 2015, Meta-analysis of the efficacy and safety of Ginkgo biloba extract for the treatment of dementia, J. Pharm. Health Care Sci. source

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    Premisecitation

    In a double-blind, randomized, placebo-controlled study of 28 healthy subjects, Centella asiatica extract administered twice a day for two months at 250, 500, and 750 mg dosages enhanced working memory at the highest dosage and improved self-rated mood post-treatment.

    “The experimental results elucidate that the highest dosage indeed enhanced working memory, and improvements in self-rated mood were also noted post-treatment, implying that C. asiatica could be helpful in mitigating age-associated cognitive impairment while also boosting mood in healthy geriatric subjects [136].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [136] Wattanathorn, 2008, Positive modulation of cognition and mood in the healthy elderly volunteer following the administration of Centella asiatica, J. Ethnopharmacol. source

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    Premisecitation

    Proposed mechanisms of Ginkgo biloba extract include beta-amyloid peptide aggregation inhibitory effects, antioxidant activities, antiplatelet-activating factor activity, and reduced expression of the peripheral benzodiazepine receptor.

    “The proposed mechanisms of G. biloba extract include Beta-amyloid peptide aggregation inhibitory effects, antioxidant activities, antiplatelet-activating factor activity, and reduced expression of the peripheral benzodiazepine receptor, which is helpful for stress relief [120,121,122].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [120] Bastianetto, 2000, The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid, Eur. J. Neurosci. source

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    • cites [121] Ryu, 2009, Ginkgo biloba extract enhances antiplatelet and antithrombotic effects of cilostazol without prolongation of bleeding time, Thromb. Res. source

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    • cites [122] Amri, 1996, In vivo regulation of peripheral-type benzodiazepine receptor and glucocorticoid synthesis by Ginkgo biloba extract EGb 761 and isolated ginkgolides, Endocrinology source

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    Premisecitation

    Ginkgo biloba extract reverses nitric oxide and beta-amyloid toxicity in vitro while decreasing apoptosis in vivo and in vitro.

    “G. biloba extract has been shown to reverse nitric oxide and Beta-amyloid toxicity in vitro while simultaneously decreasing apoptosis in vivo and in vitro [120,123,124].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [120] Bastianetto, 2000, The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid, Eur. J. Neurosci. source

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    • cites [123] Smith, 2002, Anti-apoptotic properties of Ginkgo biloba extract EGb 761 in differentiated PC12 cells, Cell. Mol. Biol.

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    • cites [124] Bastianetto, 2000, The Ginkgo biloba extract (EGb 761) protects and rescues hippocampal cells against nitric oxide-induced toxicity: Involvement of its flavonoid constituents and protein kinase C, J. Neurochem. source

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    Premisecitation

    Ginkgo biloba extract has demonstrated ameliorative effects in Alzheimer's disease, tinnitus, and cancer treatments.

    “G. biloba extract has demonstrated ameliorative effects in AD, tinnitus, and cancer treatments [117,118,119].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [117] Yang, 2016, Ginkgo Biloba for Mild Cognitive Impairment and Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials, Curr. Top. Med. Chem. source

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    • cites [118] Yang, 2017, Ginkgo biloba in the treatment of tinnitus: An updated literature review, Int. Tinnitus J.

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    • cites [119] Park, 2013, Chemopreventive effects of Ginkgo biloba extract in estrogen-negative human breast cancer cells, Arch. Pharm. Res. source

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    Premisecitation

    In a meta-analysis of nine studies, standard mean differences in seven studies favored Ginkgo biloba treatment over placebo, although two studies did not show statistically significant differences between Ginkgo biloba and placebo in ADAS-Cog.

    “Their meta-analysis showed that the standard mean differences in seven of the studies favored G. biloba treatment over the administered placebo, although two of the studies did not show statistically significant differences between G. biloba and placebo treatment in ADAS-Cog [128].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [128] Hashiguchi, 2015, Meta-analysis of the efficacy and safety of Ginkgo biloba extract for the treatment of dementia, J. Pharm. Health Care Sci. source

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    Premisecitation

    Ethanolic extracts of Centella asiatica elicit neurite outgrowths in SH-SY5Y human cells in the presence of nerve growth factor and expedite regeneration of axons in rats.

    “Ethanolic extracts of C. asiatica have also elicited neurite outgrowths in SH-SY5Y human cells in the presence of the nerve growth factor and expedited regeneration of the axons in rats [63].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [63] Soumyanath, 2012, Centella asiatica Extract Improves Behavioral Deficits in a Mouse Model of Alzheimer’s Disease: Investigation of a Possible Mechanism of Action, Int. J. Alzheimer’s Dis.

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Treatment with Ginkgo biloba extract improves spatial learning and memory of aluminum-intoxicated rats, potentially due to reduced APP expression and caspase-3 in the brains of treated rats.

    “Therapeutic treatment with G. biloba extract has also shown the ability to improve spatial learning and memory of aluminum-intoxicated rats, potentially due to a reduced APP expression and caspase-3 in the brains of treated-rats [125].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [125] Gong, 2005, Protective effects of Ginkgo biloba leaf extract on aluminum-induced brain dysfunction in rats, Life Sci. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Metals trigger oxidative neurotoxicity and amyloid aggregation.

    “The metals are found concentrated in AD-affected brains and trigger oxidative neurotoxicity and amyloid aggregation [167].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [167] Santos, 2016, Metals and Neuronal Metal Binding Proteins Implicated in Alzheimer’s Disease, Oxid. Med. Cell Longev. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Curcumin derivatives were all effective at decreasing plaque-associated pathology and enhancing cognitive function, despite differing improved outcomes based on the disease model.

    “Even though the derivatives provided differing improved outcomes based on the disease model, they were all effective at decreasing plaque-associated pathology and enhancing cognitive function [160,161,162].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [160] Katsori, 2011, Curcumin analogues as possible anti-proliferative & anti-inflammatory agents, Eur. J. Med. Chem. source

      Not checked in the free run.

    • cites [161] Wan, 2019, A Curcumin Analog Reduces Levels of the Alzheimer’s Disease-Associated Amyloid-β Protein by Modulating AβPP Processing and Autophagy, J. Alzheimer’s Dis. source

      Not checked in the free run.

    • cites [162] Voulgaropoulou, 2019, The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies, Brain Res. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Curcumin forms strong metal complexes, thereby blocking metal-induced Aβ inflammation, toxicity, and aggregation.

    “Curcumin has been shown to produce strong metal complexes, thereby blocking mentally induced Aβ inflammation, toxicity, and aggregation [163,168].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [163] Baum, 2004, Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer’s disease animal models, J. Alzheimer’s Dis. source

      Not checked in the free run.

    • cites [168] Yan, F.S., Sun, J.L., Xie, W.H., Shen, L., and Ji, H.F. (2017). Neuroprotective Effects and Mechanisms of Curcumin-Cu(II) and -Zn(II) Complexes Systems and Their Pharmacological Implications. Nutrients, 10. source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Interpretationcitation

    Saffron's ability to treat mild to moderate Alzheimer's disease could potentially be due to its inhibitory activity towards deposition and aggregation of beta-amyloid plaques.

    “The researchers proposed that saffron’s ability to treat mild to moderate AD could potentially be due to its inhibitory activity towards deposition and aggregation of beta-amyloid plaques [69].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [69] Akhondzadeh, 2010, A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease, Psychopharmacology source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a double-blind, randomized, controlled clinical trial of 54 Persian-speaking subjects with mild to moderate Alzheimer's disease over 22 weeks, saffron 30 mg/day had similar effects in enhancing cognitive function and less side effects compared to donepezil 10 mg/day.

    “After the conclusion of the study, it was determined that saffron had similar effects in enhancing cognitive function and less side effects in comparison to donepezil [69].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [69] Akhondzadeh, 2010, A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease, Psychopharmacology source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Curcumin decreased the deposits of amyloid-beta, potentially via autophagy promotion.

    “Likewise, curcumin decreased the deposits of Aβ, potentially via autophagy promotion [156].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [156] Wang, 2014, Downregulation of PI3K/Akt/mTOR signaling pathway in curcumin-induced autophagy in APP/PS1 double transgenic mice, Eur. J. Pharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In vitro studies show curcumin neutralizes reactive oxygen species and blocks lipid peroxidation, with curcumin having greater potency than vitamin E.

    “In vitro studies have elucidated that curcumin has the ability to neutralize reactive oxygen species and block lipid peroxidation, with curcumin being determined to have a greater potency than vitamin E [150,151].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [150] Epstein, 2010, Curcumin as a therapeutic agent: The evidence from in vitro, animal and human studies, Br. J. Nutr. source

      Not checked in the free run.

    • cites [151] Maheshwari, 2006, Multiple biological activities of curcumin: A short review, Life Sci. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Curcumin is associated with reduced inflammation, amyloid pathology, and oxidative damage in mice models of Alzheimer's disease.

    “Additionally, curcumin was also associated with reduced inflammation, amyloid pathology, and oxidative damage in mice models of AD [152,153].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [152] Yang, 2005, Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo, J. Biol. Chem. source

      Not checked in the free run.

    • cites [153] Lim, 2001, The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse, J. Neurosci. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Saffron could be considered an herbal spice with the ability to enhance completing activities of daily living as well as boosting cognitive functions in subjects with mild cognitive impairment and Alzheimer's disease.

    “Due to these studies, saffron could be considered an herbal spice with the ability to enhance the completing activities of daily living as well as boosting cognitive functions in subjects with MCI and AD [69,141,142].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [69] Akhondzadeh, 2010, A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease, Psychopharmacology source

      Not checked in the free run.

    • cites [141] Akhondzadeh, 2010, Saffron in the treatment of patients with mild to moderate Alzheimer’s disease: A 16-week, randomized and placebo-controlled trial, J. Clin. Pharm. Ther. source

      Not checked in the free run.

    • cites [142] Farokhnia, 2014, Comparing the efficacy and safety of Crocus sativus L. with memantine in patients with moderate to severe Alzheimer’s disease: A double-blind randomized clinical trial, Hum. Psychopharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Administering curcumin via peripheral injections crossed the blood-brain barrier and decreased plaque levels and blocked subsequent plaque development.

    “Likewise, administering curcumin via peripheral injections crossed the blood–brain barrier and decreased plaque levels and blocked subsequent plaque development [152].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [152] Yang, 2005, Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo, J. Biol. Chem. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a double-blind, randomized, parallel-group study of 68 subjects with moderate to severe Alzheimer's disease, saffron extract 30 mg/day was comparable with memantine 20 mg/day in decreasing cognitive decline and had a seemingly low adverse effect rate over 12 months.

    “The saffron extract was comparable with memantine in decreasing cognitive decline and had a seemingly low adverse effect rate in subjects with moderate to severe AD [142].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [142] Farokhnia, 2014, Comparing the efficacy and safety of Crocus sativus L. with memantine in patients with moderate to severe Alzheimer’s disease: A double-blind randomized clinical trial, Hum. Psychopharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Saffron demonstrated no severe or prominent adverse effects, making it a suitable natural therapeutic for these patients.

    “Subsequently, the studies demonstrated no severe or prominent adverse effects, making saffron a suitable natural therapeutic for these patients.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [69] Akhondzadeh, 2010, A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease, Psychopharmacology source

      Not checked in the free run.

    • cites [141] Akhondzadeh, 2010, Saffron in the treatment of patients with mild to moderate Alzheimer’s disease: A 16-week, randomized and placebo-controlled trial, J. Clin. Pharm. Ther. source

      Not checked in the free run.

    • cites [142] Farokhnia, 2014, Comparing the efficacy and safety of Crocus sativus L. with memantine in patients with moderate to severe Alzheimer’s disease: A double-blind randomized clinical trial, Hum. Psychopharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a double-transgenic APP/PS1 Alzheimer's disease model, both 160 ppm low-dose and 1000 ppm high-dose curcumin for 6 months reported significant cognitive enhancement, but the higher curcumin dosage generated better cognitive improvement.

    “Both doses reported significant cognitive enhancement, but the higher curcumin dosage generated better cognitive improvement [156].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [156] Wang, 2014, Downregulation of PI3K/Akt/mTOR signaling pathway in curcumin-induced autophagy in APP/PS1 double transgenic mice, Eur. J. Pharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Allium sativum (aged garlic extract) is a potent anti-neuroinflammatory, antioxidant, and regulator of neurotransmitter signaling, which could ameliorate AD pathogenesis.

    “To illustrate this, Allium sativum in the Alliaceae family has shown to be a potent anti-neuroinflammatory, antioxidant, and regulator of neurotransmitter signaling when referring to aged garlic extract, which could ameliorate AD pathogenesis [180,181].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [180] Chauhan, 2003, Anti-amyloidogenic effect of Allium sativum in Alzheimer’s transgenic model Tg2576, J. Herb. Pharmacother. source

      Not checked in the free run.

    • cites [181] Ray, 2011, The “aged garlic extract” (AGE) and one of its active ingredients S-allyl-L-cysteine (SAC) as potential preventive and therapeutic agents for Alzheimer’s disease (AD), Curr. Med. Chem. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Juice and extracts from Punica granatum have shown neuroprotective effects in animal models, potentially by counteracting oxidative damage, minimizing inflammation of the brain and soluble Aβ42 and hippocampal amyloid deposition.

    “Likewise, juice and extracts from Punica granatum have also shown neuroprotective effects in animal models, potentially by counteracting oxidative damage, minimizing inflammation of the brain and soluble Aβ 42 and hippocampal amyloid deposition [182,183].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [182] Choi, 2011, Punica granatum protects against oxidative stress in PC12 cells and oxidative stress-induced Alzheimer’s symptoms in mice, J. Med. Food source

      Not checked in the free run.

    • cites [183] Ahmed, 2014, Pomegranate extract modulates processing of amyloid-β precursor protein in an aged Alzheimer’s disease animal model, Curr. Alzheimer Res. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    A large amount of evidence has shown that various herbs and natural bioactive products could be effective in AD treatment while having minimal severe adverse effects.

    “In general, a large amount of evidence has shown that various herbs and natural bioactive products could be effective in AD treatment while having minimal severe adverse effects [201].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [201] Akhondzadeh, 2006, Herbal medicine in the treatment of Alzheimer’s disease, Am. J. Alzheimer’s Dis. Other Demen. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Intranasal administration has limitations including a particularly small volume of administered drugs, limited surface area in the olfactory epithelium, and a relatively short retention time for drug absorption.

    “However, this method also has some limitations, such as a particularly small volume of administrated drugs, the limited surface area in the olfactory epithelium, and a relatively short retention time for drug absorption [199,200].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [199] Bors, 2018, Evaluation of intranasal delivery route of drug administration for brain targeting, Brain Res. Bull. source

      Not checked in the free run.

    • cites [200] Wu, 2008, From nose to brain: Understanding transport capacity and transport rate of drugs, Expert Opin. Drug Deliv. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Benefits of intranasal delivery include brain injury avoidance, surmounting the requirement of implanting delivery devices, and reducing systemic-administration-associated side effects.

    “The benefits of intranasal delivery comprise brain injury avoidance, surmounting the requirement of implanting delivery devises, and reducing the systemic-administration-associated side effects [196,197].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [196] Onur, 2004, Nasal route and drug delivery systems, Pharm. World Sci. source

      Not checked in the free run.

    • cites [197] Keller, 2021, Intranasal drug delivery: Opportunities and toxicologic challenges during drug development, Drug Deliv. Transl. Res.

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Intranasal administration is an efficient and noninvasive administration route that could bypass the BBB and directly target the central nervous system.

    “Thus, intranasal administration is an efficient and noninvasive administration route that could bypass the BBB and directly target the central nervous system [196].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [196] Onur, 2004, Nasal route and drug delivery systems, Pharm. World Sci. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Curcumin and resveratrol are chemically unstable.

    “Additionally, some limitations include chemical instability, since curcumin and resveratrol are chemically unstable [204].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [204] Renaud, J., and Martinoli, M.G. (2019). Considerations for the Use of Polyphenols as Therapies in Neurodegenerative Diseases. Int. J. Mol. Sci., 20. source

      Not checked in the free run.

52 of 52

  • The paper relies on this without support.

    Clinical studies of curcumin are limited in number.

    “Nonetheless, clinical studies conducted utilizing curcumin have been limited in number.”

  • The paper relies on this without support.

    In vitro and in vivo studies of other medicinal plants are limited, with most data deriving from observational studies.

    “Nonetheless, in vitro and in vivo studies are limited, with most data deriving from observational studies.”

  • The paper relies on this without support.

    Herbal components have rapid metabolism, limited solubility in aqueous environment, and incomplete distribution in the central nervous system.

    “Furthermore, rapid metabolism, limited solubility in aqueous environment, and incomplete distribution in the CNS are further limits that must be overcome.”

  • The paper relies on this without support.

    The most common administration route is oral.

    “In general, the most common administration route is oral, but it has not been clearly elucidated whether herbal components can access the central nervous system from systemic circulation.”

  • The paper relies on this without support.

    It is unclear whether herbal components can access the central nervous system from systemic circulation.

    “In general, the most common administration route is oral, but it has not been clearly elucidated whether herbal components can access the central nervous system from systemic circulation.”
5 of 5

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Mouse study counted as evidence of benefit in people with MCI

    Minor

    The conclusion attributes improved memory and executive function in subjects with mild cognitive impairment to two studies cited as [91,94]. The paper describes study [91] as research in APP/PS1 mice, not people with MCI.

1 of 1

Cites

1 retracted

Flagged first, then by citations

14 of the 222 references couldn’t be matched to a known paper.

Cited by

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Related

Authors
Zieneldien, T., Kim, J., & Cao, C.
Affiliations
University of South Florida (US)
Corresponding author
Cao, Chuanhai
ORCID
Venue
Geriatrics
Publisher
MDPI AG
Published
2022-02-26
Volume
7
Issue
2
Pages
24
ISSN
2308-3417 (ISSN-L)
DOI
10.3390/geriatrics7020024
PMC
PMC8938774
OpenAlex
W4214654618
Semantic Scholar
c55e92f2d904b668926cc95c72ddb63c06231c83
Cited by
29
References
222
Citations by year
2026: 5 · 2025: 5 · 2024: 4 · 2023: 12 · 2022: 3
FWCI
1.39
Type
journal article
Language
en
Open access
Licence
Locations
  • Geriatrics (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
Keywords
Alzheimer's disease, herbal plant extracts, medicinal plants, neurodegeneration, antioxidants, anti-inflammatory activity, cognitive enhancement, amyloid beta degradation, therapeutic target, drug discovery

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-10.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-10.

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