Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease
This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting. One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated w...
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| Veröffentlicht in: | Annals of neurology 2024-08, Vol.96 (2), p.262-275 |
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| creator | Saarinen, Emmi K Kuusimäki, Tomi Lindholm, Kari Niemi, Kalle Honkanen, Emma A Noponen, Tommi Seppänen, Marko Ihalainen, Toni Murtomäki, Kirsi Mertsalmi, Tuomas Jaakkola, Elina Myller, Elina Eklund, Mikael Nuuttila, Simo Levo, Reeta Chaudhuri, Kallol Ray Antonini, Angelo Vahlberg, Tero Lehtonen, Marko Joutsa, Juho Scheperjans, Filip Kaasinen, Valtteri |
| description | This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting.
One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [
I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling.
Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen.
Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. ANN NEUROL 2024. |
| doi_str_mv | 10.1002/ana.26957 |
| format | Article |
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One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [
I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling.
Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen.
Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. ANN NEUROL 2024.</description><identifier>ISSN: 0364-5134</identifier><identifier>ISSN: 1531-8249</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.26957</identifier><identifier>PMID: 38767012</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Binding ; Blood ; Blood levels ; Caffeine ; Coffee ; Computed tomography ; Consumption ; Dietary intake ; Disease control ; Dopamine ; Dopamine receptors ; Dopamine transporter ; Emission analysis ; Human motion ; Medical imaging ; Metabolites ; Movement disorders ; Neostriatum ; Neurodegenerative diseases ; Neuroimaging ; Parkinson's disease ; Photon emission ; Putamen ; Risk management ; Signs and symptoms ; Single photon emission computed tomography</subject><ispartof>Annals of neurology, 2024-08, Vol.96 (2), p.262-275</ispartof><rights>2024 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.</rights><rights>2024. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c308t-f0966325da27e8e0478602796a7c43a66e32e83ad16b022677054d590bb055763</cites><orcidid>0000-0002-5611-0466 ; 0000-0002-4829-7275 ; 0000-0003-3960-0815 ; 0000-0002-1749-7936 ; 0000-0003-2815-0505 ; 0000-0002-3446-7093 ; 0009-0003-2371-3230 ; 0000-0002-8003-1346 ; 0000-0001-5759-1911 ; 0000-0003-1005-7812 ; 0000-0001-9502-7131 ; 0000-0003-3497-5706 ; 0000-0003-1040-2807 ; 0000-0002-3457-9415</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38767012$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saarinen, Emmi K</creatorcontrib><creatorcontrib>Kuusimäki, Tomi</creatorcontrib><creatorcontrib>Lindholm, Kari</creatorcontrib><creatorcontrib>Niemi, Kalle</creatorcontrib><creatorcontrib>Honkanen, Emma A</creatorcontrib><creatorcontrib>Noponen, Tommi</creatorcontrib><creatorcontrib>Seppänen, Marko</creatorcontrib><creatorcontrib>Ihalainen, Toni</creatorcontrib><creatorcontrib>Murtomäki, Kirsi</creatorcontrib><creatorcontrib>Mertsalmi, Tuomas</creatorcontrib><creatorcontrib>Jaakkola, Elina</creatorcontrib><creatorcontrib>Myller, Elina</creatorcontrib><creatorcontrib>Eklund, Mikael</creatorcontrib><creatorcontrib>Nuuttila, Simo</creatorcontrib><creatorcontrib>Levo, Reeta</creatorcontrib><creatorcontrib>Chaudhuri, Kallol Ray</creatorcontrib><creatorcontrib>Antonini, Angelo</creatorcontrib><creatorcontrib>Vahlberg, Tero</creatorcontrib><creatorcontrib>Lehtonen, Marko</creatorcontrib><creatorcontrib>Joutsa, Juho</creatorcontrib><creatorcontrib>Scheperjans, Filip</creatorcontrib><creatorcontrib>Kaasinen, Valtteri</creatorcontrib><title>Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting.
One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [
I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling.
Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen.
Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. 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Kuusimäki, Tomi ; Lindholm, Kari ; Niemi, Kalle ; Honkanen, Emma A ; Noponen, Tommi ; Seppänen, Marko ; Ihalainen, Toni ; Murtomäki, Kirsi ; Mertsalmi, Tuomas ; Jaakkola, Elina ; Myller, Elina ; Eklund, Mikael ; Nuuttila, Simo ; Levo, Reeta ; Chaudhuri, Kallol Ray ; Antonini, Angelo ; Vahlberg, Tero ; Lehtonen, Marko ; Joutsa, Juho ; Scheperjans, Filip ; Kaasinen, Valtteri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c308t-f0966325da27e8e0478602796a7c43a66e32e83ad16b022677054d590bb055763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Binding</topic><topic>Blood</topic><topic>Blood levels</topic><topic>Caffeine</topic><topic>Coffee</topic><topic>Computed tomography</topic><topic>Consumption</topic><topic>Dietary intake</topic><topic>Disease control</topic><topic>Dopamine</topic><topic>Dopamine receptors</topic><topic>Dopamine transporter</topic><topic>Emission analysis</topic><topic>Human motion</topic><topic>Medical imaging</topic><topic>Metabolites</topic><topic>Movement disorders</topic><topic>Neostriatum</topic><topic>Neurodegenerative diseases</topic><topic>Neuroimaging</topic><topic>Parkinson's disease</topic><topic>Photon emission</topic><topic>Putamen</topic><topic>Risk management</topic><topic>Signs and symptoms</topic><topic>Single photon emission computed tomography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saarinen, Emmi K</creatorcontrib><creatorcontrib>Kuusimäki, Tomi</creatorcontrib><creatorcontrib>Lindholm, Kari</creatorcontrib><creatorcontrib>Niemi, Kalle</creatorcontrib><creatorcontrib>Honkanen, Emma A</creatorcontrib><creatorcontrib>Noponen, Tommi</creatorcontrib><creatorcontrib>Seppänen, Marko</creatorcontrib><creatorcontrib>Ihalainen, Toni</creatorcontrib><creatorcontrib>Murtomäki, Kirsi</creatorcontrib><creatorcontrib>Mertsalmi, Tuomas</creatorcontrib><creatorcontrib>Jaakkola, Elina</creatorcontrib><creatorcontrib>Myller, Elina</creatorcontrib><creatorcontrib>Eklund, Mikael</creatorcontrib><creatorcontrib>Nuuttila, Simo</creatorcontrib><creatorcontrib>Levo, Reeta</creatorcontrib><creatorcontrib>Chaudhuri, Kallol Ray</creatorcontrib><creatorcontrib>Antonini, Angelo</creatorcontrib><creatorcontrib>Vahlberg, Tero</creatorcontrib><creatorcontrib>Lehtonen, Marko</creatorcontrib><creatorcontrib>Joutsa, Juho</creatorcontrib><creatorcontrib>Scheperjans, Filip</creatorcontrib><creatorcontrib>Kaasinen, Valtteri</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saarinen, Emmi K</au><au>Kuusimäki, Tomi</au><au>Lindholm, Kari</au><au>Niemi, Kalle</au><au>Honkanen, Emma A</au><au>Noponen, Tommi</au><au>Seppänen, Marko</au><au>Ihalainen, Toni</au><au>Murtomäki, Kirsi</au><au>Mertsalmi, Tuomas</au><au>Jaakkola, Elina</au><au>Myller, Elina</au><au>Eklund, Mikael</au><au>Nuuttila, Simo</au><au>Levo, Reeta</au><au>Chaudhuri, Kallol Ray</au><au>Antonini, Angelo</au><au>Vahlberg, Tero</au><au>Lehtonen, Marko</au><au>Joutsa, Juho</au><au>Scheperjans, Filip</au><au>Kaasinen, Valtteri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2024-08-01</date><risdate>2024</risdate><volume>96</volume><issue>2</issue><spage>262</spage><epage>275</epage><pages>262-275</pages><issn>0364-5134</issn><issn>1531-8249</issn><eissn>1531-8249</eissn><abstract>This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting.
One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [
I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling.
Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen.
Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. ANN NEUROL 2024.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>38767012</pmid><doi>10.1002/ana.26957</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-5611-0466</orcidid><orcidid>https://orcid.org/0000-0002-4829-7275</orcidid><orcidid>https://orcid.org/0000-0003-3960-0815</orcidid><orcidid>https://orcid.org/0000-0002-1749-7936</orcidid><orcidid>https://orcid.org/0000-0003-2815-0505</orcidid><orcidid>https://orcid.org/0000-0002-3446-7093</orcidid><orcidid>https://orcid.org/0009-0003-2371-3230</orcidid><orcidid>https://orcid.org/0000-0002-8003-1346</orcidid><orcidid>https://orcid.org/0000-0001-5759-1911</orcidid><orcidid>https://orcid.org/0000-0003-1005-7812</orcidid><orcidid>https://orcid.org/0000-0001-9502-7131</orcidid><orcidid>https://orcid.org/0000-0003-3497-5706</orcidid><orcidid>https://orcid.org/0000-0003-1040-2807</orcidid><orcidid>https://orcid.org/0000-0002-3457-9415</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Binding Blood Blood levels Caffeine Coffee Computed tomography Consumption Dietary intake Disease control Dopamine Dopamine receptors Dopamine transporter Emission analysis Human motion Medical imaging Metabolites Movement disorders Neostriatum Neurodegenerative diseases Neuroimaging Parkinson's disease Photon emission Putamen Risk management Signs and symptoms Single photon emission computed tomography |
| title | Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease |
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