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Curcumin stains amyloid plaques like thioflavin S in AD and Tg2576 brain sections. A and B, adjacent sections from 22-month APPsw Tg2576 brain; C and D, adjacent sections of AD hippocampus. E is from the same section as B, but the right half of the field was exposed for 3 min longer than the left half of the field. The arrows point to lipofuscin. A and C are stained with 1% thioflavin S, whereas B–E are labeled with curcumin (1 M). Curcumin fluorochromes produce orange to yellow/green fluorescent plaques, and thioflavin S results in much better tangle staining. A and B, bar, 80 m; C–E, bar, 25 m.
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Alzheimer's disease (AD) involves amyloid beta (Abeta) accumulation, oxidative damage, and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive defic...
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... curcumin is a fluorochrome, we first compared plaque-associated curcumin fluorescence with that of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. ...
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... curcumin is a fluorochrome, we first compared plaque-associated curcumin fluorescence with that of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly ...
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... curcumin is a fluorochrome, we first compared plaque-associated curcumin fluorescence with that of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). ...
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... curcumin is a fluorochrome, we first compared plaque-associated curcumin fluorescence with that of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged ...
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... compared plaque-associated curcumin fluorescence with that of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged (2-min) light exposure, the fluorescence gradually shifted to yellow/green ...
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... of thioflavin S, using sections from APPsw (Tg2576) mouse brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged (2-min) light exposure, the fluorescence gradually shifted to yellow/green fluorescence. This phenomenon is illustrated in Fig. 2E, where ...
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... brain (Fig. 2, A, B, and E) and AD hippocampus (Fig. 2, C and D). Like thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged (2-min) light exposure, the fluorescence gradually shifted to yellow/green fluorescence. This phenomenon is illustrated in Fig. 2E, where the right side of the field was illuminated for 3 min ...
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... thiofla- vin S (Fig. 2, A and C), curcumin brightly labeled amyloid plaques (1 M; Fig. 2, B-E). In AD brain, curcumin labeled plaques with a yellow fluorescence (Fig. 2D) similar to thiofla- vin S in an adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged (2-min) light exposure, the fluorescence gradually shifted to yellow/green fluorescence. This phenomenon is illustrated in Fig. 2E, where the right side of the field was illuminated for 3 min before shifting the field back to make the photoexposure. Color change ...
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... adjacent section (Fig. 2C). Thioflavin S labeled tangles very strongly (Fig. 2C), whereas curcumin labeled tan- gles only weakly or not at all (Fig. 2D). Curcumin fluorescence was initially yellow-orange, but with prolonged (2-min) light exposure, the fluorescence gradually shifted to yellow/green fluorescence. This phenomenon is illustrated in Fig. 2E, where the right side of the field was illuminated for 3 min before shifting the field back to make the photoexposure. Color change depended on the intensity of plaque staining and the fluores- cent exposure time, and was stable for several weeks at 4 °C. Lipofuscin age pigments in this aged mouse brain (small ar- rows) are orange/red ...
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... lane 1). When A42 was allowed to aggregate without curcumin or CR, two bands between 14.3 and 20 kDa representing the 4 -5-mer and an aggregated oligomer smear at 44 -127 kDa were also present (lane 2). As the curcumin dose increased from 0 to 4 M, the amount of higher molecular mass aggregated smear decreased as the amount of monomer A increased (Fig. 6, C and D, lanes 2-5). When curcumin was present at 16 and 64 M, the oligomeric A bands (14.3-127 kDa) disappeared, whereas the monomeric A (lanes 6 and 7) remained similar to the unaggregated A in lane 1. At 16 and 64 M, CR could reduce the oligomeric smear but not the 4 -5-mer A band. Together, these data imply that nontoxic curcumin can inhibit A42 ...
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... on protonated antipa- rallel A. This charge can be replaced by polar groups such as those present in chrysamine G, making it more brain-perme- able than CR (10) (Fig. 1). RS-0406, which was selected by high throughput screening, has analogous polar groups spaced by a hydrophobic bridge. Curcumin is similar to CR, since it can also bind to plaques (Fig. 2), prevent oligomer formation at similar low ID 50 , and recognize secondary structure in fibrillar and oligomeric A. However, like chrysamine G, curcumin's sym- metrical phenol groups make it more brain-permeable than CR and able to cross the blood-brain barrier to bind to plaques in vivo (Fig. ...
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Ectopic cell cycle events (CCEs) mark vulnerable neuronal populations in human Alzheimer disease (AD) and are observed early in disease progression. In transgenic mouse models of AD, CCEs are found before the onset of beta-amyloid peptide (Abeta) deposition to form senile plaques, a hallmark of AD. Here, we have demonstrated that alterations in bra...
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... Oral administration of curcumin at 6 g day -1 for 4-7 weeks produced no toxicity in patients 162 . Even at high doses of 12 g day -1 , curcumin was found safe but had poor bioavailability 163,164 . In the phase I, dose escalation clinical study of liposomal curcumin (Lipocurc™), the maximum safe dosage for anti-cancer treatments in patients with metastatic or locally advanced cancer was marked down to 300 (mg m -2 ) (NCT02138955) 165 . ...
Curcumin is a biologically active phytochemical which manifests therapeutic activities in numerous health conditions, including cancer. Several curcuminoids obtained naturally and synthesized artificially also showcase anti-cancer and anti-tumorigenic effects. However, its water insolubility poses difficulties in its application to biological systems, lowering its availability in living tissues, which can be overcome by using various micro-encapsulation and nano-formulations of curcumin. When used in combination with other chemotherapeutic drugs, curcumin enhances the anti-carcinogen potential and reduces the side effects induced via chemotherapy. Structural modelling of basic pharmacophores of curcumin can enhance its biological and pharmacokinetic properties, as revealed by structure-activity relationship studies of curcumin. Various clinical trials of curcumin have proven its worth as an anti-neoplastic agent in humans, with minimal side effects. Its mechanism of action involves blockage of cell-signalling pathways and cellular enzymes, promotion of immunomodulatory effects and induction of programmed cell death in cancerous cells. Curcumin is an interesting molecule with diverse effects on various diseases, but its absolute potential has yet to be reached. Hence, more in-depth studies and clinical trials are needed. This review outlines curcumin’s chemical properties and summarizes its anti-cancer and pharmacokinetic potential.
... An in vitro and in vivo study performed in mice revealed measurable brain curcumin levels of ~1.1 µM after 1 hour of injecting 50 µM curcumin into the right carotid artery, suggesting that this polyphenol can cross the blood-brain barrier (BBB) (Yang et al., 2005). In vitro, this study also revealed that curcumin inhibits the formation of Aβ oligomers, and its effects are not determined by the specific order of amino acids in Aβ but rather by the overall structure of the fibrils. ...
... Low dosages of curcumin decreased the quantity of A plaques in the AD-afflicted mice's brains by 43%. Previous research found that for treating AD, modest doses of curcumin administered over an extended period were preferable to higher doses (Yang et al., 2005). urcumin can bind to Aβ and prevents it from self-assembling (Reinke and Gestwicki, 2007). ...
Alzheimer's Disease (AD) is a neurological disorder related to aging, considered a memory issue. Numerous research studies have been conducted to identify viable AD therapies. There isn't yet a suitable therapeutic option, though. Symptomatic behavior may help with memory loss and other dementia-related problems even though there is no known cure for AD. Since ancient times, traditional medicine has been utilized as a memory booster all across the world. Dementia, amnesia, and AD have all traditionally been treated with natural medicine, which includes herbs and botanical remedies. The use of botanical remedies in many medical systems, especially the Unani school of medicine, has long been beneficial for managing and treating memory deficits. The majority of plants and herbs have been evaluated chemically, and clinical trials have also shown their effectiveness. The underlying mechanisms for the activities, however, are still being created. In this essay, we covered several medicinal plants that are essential to the traditional herbal therapy used to treat memory loss and AD. The present review covers the literature survey from 1968 to 2023. The data have been collected from various journals, books, and some of electronic searches via Internet-based information such as PubMed, Google Scholar, ScienceDirect, EBSCO, online electronic journals, SpringerLink, Wiley, and Ayush. From the literature survey, it has been found that the herbal drug contains a wide variety of flavonoids, phenolic acids, steroids, volatile oils, lignans, alkaloids, polysaccharides, and so on. These phytochemicals exhibit a range of pharmacological activities including neurological disorders, antioxidant, and anti-inflammatory properties.
... Curcuma longa L. is a perennial herbaceous plant of the Zingiberaceae family commonly referred as turmeric and has been extensively applied for centuries in the traditional medicine of Asian countries as panacea for a series of diseases, including allergy, depression problems and cardiovascular disorders [1][2][3][4][5][6]. Modern studies have attributed the antiinflammatory, neuroprotective, antioxidant, hepatoprotective and antidiabetic properties of turmeric to curcuminoids, a class of polyphenols isolated from the rhizome of the plant, also responsible for the typical yellow color of the curry spice and often added as colorant in food [7][8][9][10][11][12][13][14]. ...
Although identical in molecular formula and weight, curcumin and cyclocurcumin show remarkable differences in their reactivity. Both are natural compounds isolated from the rhizome of turmeric, the former is involved in the diketo/keto-enol tautomerism through the bis-α,β-unsaturated diketone unit according to the polarity of the solvent, while the latter could react by trans-cis isomerization due to the presence of the α,β-unsaturated dihydropyranone moiety. Even if curcumin is generally considered responsible of the therapeutical properties of Curcuma longa L. due to its high content, cyclocurcumin has attracted great interest over the last several decades for its individual behavior and specific features as a bioactive compound. Cyclocurcumin has a hydrophobic nature characterized by fluorescence emission, solvatochromism, and the tendency to form spherical fluorescent aggregates in aqueous solution. Molecular docking analysis reveals the potentiality of cyclocurcumin as antioxidant, enzyme inhibitor, and antiviral agent. Promising biological activities are observed especially in the treatment of degenerative and cardiovascular diseases. Despite the versatility emerging from the data reported herein, the use of cyclocurcumin seems to remain limited in clinical applications mainly because of its low solubility and bioavailability.
... Another study suggested that EGCG binds to large oligomers or preformed fibrils and remodels them into less toxic forms [152]. Furthermore, curcumin in a dose dependent manner can significantly block Aβ oligomerization, inhibit fibril formation, and destabilize preexisting fibrils [153][154][155]. However, resveratrol curtails Aβ cytotoxicity by remodeling the oligomers into nontoxic assemblies but does not prevent Aβ oligomerization [53,156,157]. ...
Alzheimer’s disease (AD) is a very common neurodegenerative disorder associated with memory loss and a progressive decline in cognitive activity. The two major pathophysiological factors responsible for AD are amyloid plaques (comprising amyloid-beta aggregates) and neurofibrillary tangles (consisting of hyperphosphorylated tau protein). Polyphenols, a class of naturally occurring compounds, are immensely beneficial for the treatment or management of various disorders and illnesses. Naturally occurring sources of polyphenols include plants and plant-based foods, such as fruits, herbs, tea, vegetables, coffee, red wine, and dark chocolate. Polyphenols have unique properties, such as being the major source of anti-oxidants and possessing anti-aging and anti-cancerous properties. Currently, dietary polyphenols have become a potential therapeutic approach for the management of AD, depending on various research findings. Dietary polyphenols can be an effective strategy to tackle multifactorial events that occur with AD. For instance, naturally occurring polyphenols have been reported to exhibit neuroprotection by modulating the Aβ biogenesis pathway in AD. Many nanoformulations have been established to enhance the bioavailability of polyphenols, with nanonization being the most promising. This review comprehensively provides mechanistic insights into the neuroprotective potential of dietary polyphenols in treating AD. It also reviews the usability of dietary polyphenol as nanoformulation for AD treatment.
... Moreover, owing to their pharmacological characteristics, including neuroprotective, anti-amyloid antioxidant anti-inflammatory activities of natural agents such as curcumin (CCM) have been examined as capable agents in AD treatment [121]. The antioxidant capabilities of CCM work against the free radicals involved in neurodegenerative processes, preventing lipid peroxidation in the brain and tau protein hyperphosphorylation [122,123]. Moreover, CCM inhibits the production of proinflammatory cytokines, which affects neuroinflammation [124] and lowers the development of amyloid-beta plaques in vivo [123]. ...
... The antioxidant capabilities of CCM work against the free radicals involved in neurodegenerative processes, preventing lipid peroxidation in the brain and tau protein hyperphosphorylation [122,123]. Moreover, CCM inhibits the production of proinflammatory cytokines, which affects neuroinflammation [124] and lowers the development of amyloid-beta plaques in vivo [123]. Its water insolubility, substantial T. Zivari-Ghader et al. metabolism, limited instability, and bioavailability in the biological milieu make it difficult to use in clinical settings [125]. ...
Alzheimer's disease is a neurological disorder that causes increased memory loss, mood swings, behavioral disorders, and disruptions in daily activities. Polymer scaffolds for the brain have been grown under laboratory, physiological, and pathological circumstances because of the limitations of conventional treatments for patients with central nervous system diseases. The blood-brain barrier prevents medications from entering the brain, challenging AD treatment. Numerous biomaterials such as biomolecules, polymers, inorganic metals, and metal oxide nanoparticles have been used to transport therapeutic medicines into the nervous system. Incorporating biocompatible materials that support neurogenesis through a combination of topographical, pharmacological, and mechanical stimuli has also shown promise for the transfer of cells to replenish dopaminergic neurons. Components made of naturally occurring biodegradable polymers are appropriate for the regeneration of nerve tissue. The ability of natural-based materials (biomaterials) has been shown to promote endogenous cell development after implantation. Also, strategic functionalization of polymeric nanocarriers could be employed for treating AD. In particular, nanoparticles could resolve Aβ aggregation and thus help cure Alzheimer's disease. Drug moieties can be effectively directed to the brain by utilizing nano-based systems and diverse colloidal carriers, including hydrogels and biodegradable scaffolds. Notably, early investigations employing neural stem cells have yielded promising results, further emphasizing the potential advancements in this field. Few studies have fully leveraged the combination of cells with cutting-edge biomaterials. This study provides a comprehensive overview of prior research, highlighting Heliyon 10 (2024) e26351 2 the pivotal role of biomaterials as sophisticated drug carriers. It delves into various intelligent drug delivery systems, encompassing pH and thermo-triggered mechanisms, polymeric and lipid carriers, inorganic nanoparticles, and other vectors. The discussion synthesizes existing knowledge and underscores the transformative impact of these biomaterials in devising innovative strategies, augmenting current therapeutic methodologies, and shaping new paradigms in the realm of Alzheimer's disease treatment.
... The responsive fragments comprise the major sequences in the hydrophobic central (Aβ [13][14][15][16][17][18][19][20] , HHQKLVFF) and C-terminal (Aβ 31-42 , IIGLMVGGVVIA) regions. The central region KLVFF (Aβ [16][17][18][19][20] ) has been previously reported as the interacting domain of Aβ with curcumin analogs [44][45][46] . To visualize the spectrum of the binding sites of Q-OB on a full-length Aβ 1-42 sequence, a heatmap with a two-color gradient (white to red, 0-100%) is shown in Fig. 4b. ...
Amyloid-β (Aβ) oligomers are implicated in the onset of Alzheimer’s disease (AD). Herein, quinoline-derived half-curcumin-dioxaborine (Q-OB) fluorescent probe was designed for detecting Aβ oligomers by finely tailoring the hydrophobicity of the biannulate donor motifs in donor-π-acceptor structure. Q-OB shows a great sensing potency in dynamically monitoring oligomerization of Aβ during amyloid fibrillogenesis in vitro. In addition, we applied this strategy to fluorometrically analyze Aβ self-assembly kinetics in the cerebrospinal fluids (CSF) of AD patients. The fluorescence intensity of Q-OB in AD patients’ CSF revealed a marked change of log (I/I0) value of 0.34 ± 0.13 (cognitive normal), 0.15 ± 0.12 (mild cognitive impairment), and 0.14 ± 0.10 (AD dementia), guiding to distinguish a state of AD continuum for early diagnosis of AD. These studies demonstrate the potential of our approach can expand the currently available preclinical diagnostic platform for the early stages of AD, aiding in the disruption of pathological progression and the development of appropriate treatment strategies.
... Curcumin, a polyphenolic compound derived from turmeric, can interact with the beta-pleated sheet structure of amyloids. This interaction is a key mechanism through which curcumin contributes to reducing plaque accumulation in various models of AD pathogenesis [93] [94]. In addition, curcumin can bind to Aβ and reduce toxic aggregates by regulating amyloid aggregation. ...
Neurodegenerative diseases (NDDs), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and glioblastoma tumors (GB), represent a spectrum of disorders characterized by pro-gressive neuronal degeneration. This gradual deterioration presents significant challenges in ear-ly diagnosis and treatment. As a solution, iron oxide nanoparticles (IONPs) have emerged as promising materials due to their diminutive size and inherent biocompatibility, which facilitates bypassing the blood-brain barrier (BBB), thereby serving as effective targeted nanocarriers for neuroprotective therapeutics, offering efficient delivery to the brain. Furthermore, IONPs demonstrate efficacy as T1/T2 contrast agents (CAs), offering a novel diagnostic tool for various NDDs, emphasizing GB. Despite the expanding potential of IONPs in the management of NDDs, a clear gap exists in developing environmentally sustainable synthesis methods. Such methods must adhere to ecological standards and enable the production of nanoparticles capable of efficiently crossing the BBB. This is essential for precisely delivering and monitoring therapeutic interventions in diseases such as AD, PD, and GB. This review sys-tematically explores the potential of green-synthesized IONPs in the context of NDD treatment. In this review, we emphasize different functionalization techniques for IONPs, tackling how these functionalized IONPs can be effective therapeutic approaches for NDDs. Moreover, we discuss biosafety and biocompatibility by covering a range of in vitro biocompatibility studies to analyze the safety of green-synthesized IONPs for the human body. Furthermore, our thorough analysis discussed the current state of green-synthesized IONPs using plant extracts polyphe-nols, which also act as neuroprotective agents, as proved by studies mentioned in the review.
... "Other studies indicated that the non-steroidal antiinflammatory property of turmeric is associated with a reduced risk of AD" [44]. "It was reported to reduce oxidative damage and reversed the amyloid pathology in an AD transgenic mouse" [45,46]. "Direct injection of curcumin into the brains of the mice with AD not only hampered further development of plaque but also reduced the plaque levels" [46]. ...
... "It was reported to reduce oxidative damage and reversed the amyloid pathology in an AD transgenic mouse" [45,46]. "Direct injection of curcumin into the brains of the mice with AD not only hampered further development of plaque but also reduced the plaque levels" [46]. "Low dose of this compound further reduced the cytokines level of IL-1β" [39]. ...
Alzheimer's disease and Parkinson's disease are debilitating neurodegenerative disorders that impose a significant burden on the affected individuals and the society as a whole. Despite extensive research efforts, effective treatments for these diseases remain elusive till date. Ayurveda, a traditional system of medicinal practice which originated in ancient India, has long touted the potential of various plants possessing neuroprotective properties. The effects of a few relevant Ayurvedic plants viz. Guduchi, Kapikachhu, Shankhapushpi, Turmeric, Mandukparni, Ashwagadha, Brahmi, Jatamansi etc. on several non-human primates and rodents have been reported. The therapeutic potential of those plants to mitigate the pathological hallmarks associated with Alzheimer's disease and Parkinson's disease was assessed. We have outlined the most recent research on Ayurveda's effects on neurodegenerative brain illnesses in this review article, with an emphasis on Alzheimer's disease and Parkinson's disease. As the zebrafish (Danio rerio Hamilton) has emerged as a useful, non-mammalian vertebrate model organism for studying a wide range of diseases, the effect of few other medicinal plants on zebrafish was also mentioned. Powerful live imaging and genetic tools which is currently available for zebrafish has transformed this fish to a top model in biomedical research and toxicity testing. However, further research is needed to elucidate the precise mechanisms of action and to translate these promising results into clinical applications. The exploration of traditional medicinal systems, in conjunction with modern scientific methodologies using novel model organisms, such as zebrafish offers a valuable avenue for the development of innovative treatments for neurodegenerative disorders.
... As previously described, it is believed that one of the major causes of Alzheimer's disease is the accumulation of beta-amyloid plaques in the brain, leading to several cellular changes that leads to synaptic dysfunction. Many studies have shown positive effects of curcumin supplementation in counteracting the deleterious effects of beta-amyloid plaques [16,48]. ...
... To evaluate curcumin's inhibitory effects on beta-amyloid plaque aggregation, Yang and coauthors [48] used groups of APPsw Tg2576 transgenic mice bred on 500ppm of curcumin or safflower oil diets, aged until their 22 months of age. Prior to slaughter, a mice from the 500ppm curcumin diet was injected with 200μl of curcumin/PBS within 5 minutes. ...
... In the same study [48], it was found that in vitro, increasing doses of curcumin (0-8μM) were able to disaggregate pre-aggregated beta-amyloid. The present study also compared the beta-amyloid antiaggregating effect of curcumin with non-steroidal anti-inflammatory drugs. ...
