{"id":1577,"date":"2024-05-08T13:00:55","date_gmt":"2024-05-08T17:00:55","guid":{"rendered":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/?p=1577"},"modified":"2024-05-08T13:00:55","modified_gmt":"2024-05-08T17:00:55","slug":"saffron-can-reduce-cognitive-impairment-and-biomarkers-of-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/biology\/saffron-can-reduce-cognitive-impairment-and-biomarkers-of-alzheimers-disease\/","title":{"rendered":"Saffron Can Reduce Cognitive Impairment and Biomarkers of Alzheimer\u2019s Disease"},"content":{"rendered":"<p><span style=\"font-weight: 400\">Saffron is a popular food condiment known to have a positive effect against neurodegenerative diseases such as dementia, Alzheimer\u2019s, and Parkinson\u2019s. Saffron could potentially alleviate some of the biological hallmarks of Alzheimer\u2019s disease, including the accumulation of A\u03b2 plaques outside of cells and neurofibrillary tangles (NFTs) inside of cells. It could also target the neurotransmitter system that involves acetylcholine (ACh), which when disrupted can lead to the progression of dementia. This system, called the cholinergic system, is essential for attention, learning, and memory. ACh plays a role in memory acquisition, encoding, and consolidation (Patel et al. 2024).\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">A recent study looked at how saffron extract (CSE) supplementation affects behavioral activity, memory, A\u03b2 plaques, and NFTs in rats. The study also investigated how saffron affects a disrupted cholinergic system. When the system breaks down, there is an increase in A\u03b2 plaques and NFTs. There is also an increase in AChE, which is the protein that breaks down ACh. All of these factors can ultimately contribute to Alzheimer\u2019s. The current study investigated how CSE could reduce these effects and ultimately prevent progression of dementia-related diseases (Patel et al. 2024).\u00a0\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">In order to study the effects of CSE, the researchers used the drug scopolamine to disrupt the <\/span><span style=\"font-weight: 400\">cholinergic system in rats. Scopolamine mimics the memory loss observed in dementia, and it is often used to study the cholinergic system in animal models of dementia. It primarily impairs the acquisition and encoding of memories<\/span><span style=\"font-weight: 400\"> (Paul 2019). Scopolamine increases the level of AChE in the brain, which means that more ACh is broken down. With less ACh available, the <\/span><span style=\"font-weight: 400\">cholinergic system is disrupted, causing cognitive impairments (Figure 1). <\/span><span style=\"font-weight: 400\">The study observed the potential of CSE to reduce this disturbance. They used behavioral tests to observe memory and spatial acquisition. Blood samples and brain samples were collected for examination (Patel et al. 2024).\u00a0<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\" wp-image-1578 aligncenter\" src=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.45.46\u202fPM-300x208.png\" alt=\"\" width=\"381\" height=\"264\" srcset=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.45.46\u202fPM-300x208.png 300w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.45.46\u202fPM-1024x711.png 1024w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.45.46\u202fPM-768x534.png 768w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.45.46\u202fPM.png 1094w\" sizes=\"auto, (max-width: 381px) 100vw, 381px\" \/><\/p>\n<p><span style=\"font-weight: 400\">Figure 1. The role of acetylcholinesterase (AChE). AChE breaks down acetylcholine (ACh) as it moves from one neuron to another. An increase in AChE leads to a decrease in ACh. (Adapted from What is the role of acetylcholinesterase at a synapse?)<\/span><\/p>\n<p><span style=\"font-weight: 400\">The researchers found that CSE supplementation significantly improved behavioral activity and memory in rats. CSE improved performance on the reversal task, which requires the ability to switch between learned and new responses, a reflection of cognitive flexibility.\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">Importantly, the study offers insight into the biological parameters that lead to the improved cognitive abilities. CSE lowered the levels of AChE, meaning that less acetylcholine was broken down. The dose of 20 mg\/kg of CSE lowered the amount of AChE in the scopolamine-treated rats as significantly as Rivastigmine did (Figure 2). Rivastigmine is a pharmaceutical drug currently used to treat symptoms of Alzheimer\u2019s by inhibiting AChE (Emre et al. 2010). An increase in the level of <\/span><span style=\"font-weight: 400\">acetylcholine can improve memory, as demonstrated by the improved performance of the rats on the memory tests. ACh has been shown to promote nerve conduction related to memory and learning ability, helping memories get encoded and consolidated in the brain.\u00a0<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\" wp-image-1579 aligncenter\" src=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.47.33\u202fPM-300x194.png\" alt=\"\" width=\"394\" height=\"255\" srcset=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.47.33\u202fPM-300x194.png 300w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.47.33\u202fPM-768x497.png 768w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.47.33\u202fPM.png 958w\" sizes=\"auto, (max-width: 394px) 100vw, 394px\" \/><\/p>\n<p><span style=\"font-weight: 400\">Figure 2. CSE supplementation lowered the levels of AChE and inhibited its effects in rats who received scopolamine administration. Thus, less acetylcholine was broken down and disruption of the cholinergic system was attenuated. This can lead to an improvement in memory (Adapted from Patel et al, 2024).\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">CSE supplementation also significantly reduced the formation of <\/span><span style=\"font-weight: 400\">A\u03b2 plaques and NFTs, the two classical pathological hallmarks of Alzheimer\u2019s in the hippocampus in the brain. The 20 mg\/kg dose of CSE produced the most significant reduction. CSE reduced the number of A\u03b2 plaques and NFTs more than <\/span><span style=\"font-weight: 400\">Rivastigmine did. In fact, the Rivastigmine group still had significant levels of NFTs and <\/span><span style=\"font-weight: 400\">A\u03b2 plaques<\/span> <span style=\"font-weight: 400\">(Figure 3). Accumulation of A\u03b2 plaques and NFTs lead to neuronal dysfunction and ultimately dementia. Moreover, AChE and A\u03b2 can bind together to form complexes that exaggerate neurodegeneration even more. Thus, if CSE can attenuate their formation, neuronal function may be preserved, preventing the progression of dementia.\u00a0\u00a0<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\" wp-image-1580 aligncenter\" src=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.48.26\u202fPM-300x192.png\" alt=\"\" width=\"400\" height=\"256\" srcset=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.48.26\u202fPM-300x192.png 300w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.48.26\u202fPM-768x492.png 768w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.48.26\u202fPM.png 996w\" sizes=\"auto, (max-width: 400px) 100vw, 400px\" \/><\/p>\n<p><span style=\"font-weight: 400\">Figure 3. CSE supplementation lowered the density of <\/span><span style=\"font-weight: 400\">A\u03b2 plaques<\/span><span style=\"font-weight: 400\"> in rats who received scopolamine administration. This can lead to an improvement in memory (Adapted from Patel et al, 2024).\u00a0<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\" wp-image-1581 aligncenter\" src=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-300x201.png\" alt=\"\" width=\"486\" height=\"326\" srcset=\"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-300x201.png 300w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-1024x688.png 1024w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-768x516.png 768w, https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM.png 1474w\" sizes=\"auto, (max-width: 486px) 100vw, 486px\" \/><\/p>\n<p><span style=\"font-weight: 400\">Figure 4. Summary of the article. Scopolamine administration led to a disruption of the cholinergic system (a part of the nervous system involving acetylcholine that helps with memory and learning), neuroinflammation, and accumulation of NFT and A\u03b2 plaques. When CSE (saffron extract) was administered, the rats\u2019 memory improved and the biomarkers of Alzheimer\u2019s were reduced (Adapted from Patel et al, 2024).\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">Because CSE supplementation reduces the formation of <\/span><span style=\"font-weight: 400\">A\u03b2 plaque and NFTs in the hippocampus, inhibits the activity of the enzyme that breaks down acetylcholine, and counters neuroinflammation, a saffron-based botanical supplement could be used to help manage dementia. Currently, manufactured drugs such as donepezil and memantine have been used to treat symptoms of Alzheimer\u2019s, but saffron could potentially offer a safer alternative that is just as effective (D\u2019Onofrio et al. 2021). The current study tested the effects of CSE against Rivastigmine, another drug that is approved to treat symptoms of Alzheimer\u2019s. CSE produced the same improvements as Rivastigmine. Rivastigmine, along with other chemical drugs that inhibit AChE in order to treat Alzheimer\u2019s, has been shown to cause gastrointestinal side effects and does not have great patient compliance (Emre et al. 2010). Saffron supplementation could offer an effective treatment without such side effects, increasing quality of life. The research offers promise that saffron can improve the cognitive impairments associated with Alzheimer\u2019s and dementia.\u00a0<\/span><\/p>\n<p>&nbsp;<\/p>\n<p style=\"text-align: center\"><span style=\"font-weight: 400\">Literature Cited<\/span><\/p>\n<p><span style=\"font-weight: 400\">Emre M, Bernabei R, Blesa R, Bullock R, Cunha L, Dani\u00ebls H, Dziadulewicz E, F\u00f6rstl H, Fr\u00f6lich L, Gabryelewicz T, et al. 2010. Drug Profile: Transdermal Rivastigmine Patch in the Treatment of Alzheimer Disease. CNS Neurosci Ther. 16(4):246\u2013253.\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">D\u2019Onofrio G, Nabavi SM, Sancarlo D, Greco A, Pieretti S. 2021. Crocus Sativus L. (Saffron) in Alzheimer\u2019s Disease Treatment: Bioactive Effects on Cognitive Impairment. Curr Neuropharmacol. 19(9):1606\u20131616.\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">Patel KS, Dharamsi A, Priya M, Jain S, Mandal V, Girme A, Modi SJ, Hingorani L. 2024a. Saffron (<\/span><i><span style=\"font-weight: 400\">Crocus sativus<\/span><\/i><span style=\"font-weight: 400\"> L.) extract attenuates chronic scopolamine-induced cognitive impairment, amyloid beta, and neurofibrillary tangles accumulation in rats. Journal of Ethnopharmacology. 326:117898.\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">Paul J. 2019. Chapter 5 &#8211; Experimental Medicine Approaches in CNS Drug Development. In: Nomikos GG, Feltner DE, editors. Handbook of Behavioral Neuroscience. Vol. 29. Elsevier. (Translational Medicine in CNS Drug Development). p. 63\u201380. [accessed 2024 Feb 25].\u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">What is the role of acetylcholinesterase at a synapse? | Socratic. Socratic.org. [accessed 2024 Mar 21].<\/span><a href=\"https:\/\/socratic.org\/questions\/what-is-the-role-of-acetylcholinesterase-at-a-synapse-1\"><span style=\"font-weight: 400\">\u00a0<\/span><\/a><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Saffron is a popular food condiment known to have a positive effect against neurodegenerative diseases such as dementia, Alzheimer\u2019s, and Parkinson\u2019s. Saffron could potentially alleviate some of the biological hallmarks of Alzheimer\u2019s disease, including the accumulation of A\u03b2 plaques outside of cells and neurofibrillary tangles (NFTs) inside of cells. It could also target the neurotransmitter [&hellip;]<\/p>\n","protected":false},"author":673,"featured_media":1581,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[63,68],"tags":[211,132],"class_list":{"0":"post-1577","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-biology","8":"category-psych-neuro","9":"tag-alzheimers","10":"tag-memory","11":"entry"},"featured_image_src":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-600x400.png","featured_image_src_square":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-content\/uploads\/sites\/35\/2024\/05\/Screenshot-2024-05-08-at-12.49.10\u202fPM-600x600.png","author_info":{"display_name":"Hailey Ryan '26","author_link":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/author\/hryan2\/"},"_links":{"self":[{"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/posts\/1577","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/users\/673"}],"replies":[{"embeddable":true,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/comments?post=1577"}],"version-history":[{"count":0,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/posts\/1577\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/media\/1581"}],"wp:attachment":[{"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/media?parent=1577"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/categories?post=1577"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/students.bowdoin.edu\/bowdoin-science-journal\/wp-json\/wp\/v2\/tags?post=1577"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}