Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease
IMPORTANCE: Nocturnal sleep disruption develops in Alzheimer disease (AD) owing to the derangement of the sleep-wake cycle regulation pathways. Orexin contributes to the regulation of the sleep-wake cycle by increasing arousal levels and maintaining wakefulness. OBJECTIVES: To study cerebrospinal fl...
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| Veröffentlicht in: | JAMA neurology 2014-12, Vol.71 (12), p.1498-1505 |
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| creator | Liguori, Claudio Romigi, Andrea Nuccetelli, Marzia Zannino, Silvana Sancesario, Giuseppe Martorana, Alessandro Albanese, Maria Mercuri, Nicola Biagio Izzi, Francesca Bernardini, Sergio Nitti, Alessandra Sancesario, Giulia M Sica, Francesco Marciani, Maria G Placidi, Fabio |
| description | IMPORTANCE: Nocturnal sleep disruption develops in Alzheimer disease (AD) owing to the derangement of the sleep-wake cycle regulation pathways. Orexin contributes to the regulation of the sleep-wake cycle by increasing arousal levels and maintaining wakefulness. OBJECTIVES: To study cerebrospinal fluid levels of orexin in patients with AD, to evaluate the relationship of orexin cerebrospinal fluid levels with the degree of dementia and the cerebrospinal fluid AD biomarkers (tau proteins and β-amyloid 1-42), and to analyze potentially related sleep architecture changes measured by polysomnography. DESIGN, SETTING, AND PARTICIPANTS: We conducted a case-control study from August 1, 2012, through May 31, 2013. We included 48 drug-naive AD patients referred to the Neurological Clinic of the University Hospital of Rome Tor Vergata. Based on the Mini-Mental State Examination score, 21 patients were included in mild AD group (score, ≥21), whereas 27 were included in the moderate to severe AD group (score, |
| doi_str_mv | 10.1001/jamaneurol.2014.2510 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1635004569</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><ama_id>1915582</ama_id><sourcerecordid>1635004569</sourcerecordid><originalsourceid>FETCH-LOGICAL-a326t-4908178eefebb6061c019e96e5de2705033d75bea17724590e60b4e13ef3cc5b3</originalsourceid><addsrcrecordid>eNpFkM1PAjEQxRujEYL8A8aYHj2wOG233d0jAT9ISDigVzfdZcCS_cB214h_vSUgzGXm8N6bvB8hdwyGDIA9bnSpK2xtXQw5sHDIJYML0uVMxYFiMro83WHSIX3nNuAnBghFeE06XArOOagu-Zhb_DEV2rXJ6WLnGizpZOcsrttCN6auBnRRIG7ptNxqY0usmgHV1ZKO63VlGvONdIJ54ROoqeio-P1EU6KlE-NQO7whVytdOOwfd4-8Pz-9jV-D2fxlOh7NAi24aoIwgZhFMeIKs0yBYjmwBBOFcok8AglCLCOZoWZRxEOZACrIQmQCVyLPZSZ65OGQu7X1V4uuSUvjciwKT6luXcqUkL68VImXhgdpbmvni67SrTWltruUQbqHm57hpnu46R6ut90fP7RZicuT6R-lF9weBN59jkyYlDEXf6AwgIg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1635004569</pqid></control><display><type>article</type><title>Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease</title><source>MEDLINE</source><source>American Medical Association Journals</source><creator>Liguori, Claudio ; Romigi, Andrea ; Nuccetelli, Marzia ; Zannino, Silvana ; Sancesario, Giuseppe ; Martorana, Alessandro ; Albanese, Maria ; Mercuri, Nicola Biagio ; Izzi, Francesca ; Bernardini, Sergio ; Nitti, Alessandra ; Sancesario, Giulia M ; Sica, Francesco ; Marciani, Maria G ; Placidi, Fabio</creator><creatorcontrib>Liguori, Claudio ; Romigi, Andrea ; Nuccetelli, Marzia ; Zannino, Silvana ; Sancesario, Giuseppe ; Martorana, Alessandro ; Albanese, Maria ; Mercuri, Nicola Biagio ; Izzi, Francesca ; Bernardini, Sergio ; Nitti, Alessandra ; Sancesario, Giulia M ; Sica, Francesco ; Marciani, Maria G ; Placidi, Fabio</creatorcontrib><description>IMPORTANCE: Nocturnal sleep disruption develops in Alzheimer disease (AD) owing to the derangement of the sleep-wake cycle regulation pathways. Orexin contributes to the regulation of the sleep-wake cycle by increasing arousal levels and maintaining wakefulness. OBJECTIVES: To study cerebrospinal fluid levels of orexin in patients with AD, to evaluate the relationship of orexin cerebrospinal fluid levels with the degree of dementia and the cerebrospinal fluid AD biomarkers (tau proteins and β-amyloid 1-42), and to analyze potentially related sleep architecture changes measured by polysomnography. DESIGN, SETTING, AND PARTICIPANTS: We conducted a case-control study from August 1, 2012, through May 31, 2013. We included 48 drug-naive AD patients referred to the Neurological Clinic of the University Hospital of Rome Tor Vergata. Based on the Mini-Mental State Examination score, 21 patients were included in mild AD group (score, ≥21), whereas 27 were included in the moderate to severe AD group (score, <21). The control group consisted of 29 nondemented participants of similar age and sex. EXPOSURE: Laboratory assessment of cerebrospinal fluid levels of orexin, tau proteins, and β-amyloid 1-42 and polysomnographic assessment of sleep variables. MAIN OUTCOMES AND MEASURES: Levels of orexin, tau proteins, and β-amyloid 1-42; macrostructural variables of nocturnal sleep (total sleep time, sleep efficiency, sleep onset and rapid eye movement [REM] sleep latencies, non-REM and REM sleep stages, and wakefulness after sleep onset); and Mini-Mental State Examination scores. RESULTS: Patients with moderate to severe AD presented with higher mean (SD) orexin levels compared with controls (154.36 [28.16] vs 131.03 [26.55]; P < .01) and with more impaired nocturnal sleep with respect to controls and patients with mild AD. On the other hand, in the global AD group, orexin levels were positively correlated with total tau protein levels (r = 0.32; P = .03) and strictly related to sleep impairment. Finally, cognitive impairment, as measured by the Mini-Mental State Examination, was correlated with sleep structure deterioration. CONCLUSIONS AND RELEVANCE: Our results demonstrate that, in AD, increased cerebrospinal fluid orexin levels are related to a parallel sleep deterioration, which appears to be associated with cognitive decline. Therefore, the orexinergic system seems to be dysregulated in AD, and its output and function appear to be overexpressed along the progression of the neurodegenerative process. This overexpression may result from an imbalance of the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.</description><identifier>ISSN: 2168-6149</identifier><identifier>EISSN: 2168-6157</identifier><identifier>DOI: 10.1001/jamaneurol.2014.2510</identifier><identifier>PMID: 25322206</identifier><language>eng</language><publisher>United States: American Medical Association</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer Disease - complications ; Alzheimer Disease - physiopathology ; Amyloid beta-Peptides - cerebrospinal fluid ; Case-Control Studies ; Cognition Disorders - cerebrospinal fluid ; Cognition Disorders - etiology ; Cognition Disorders - physiopathology ; Female ; Humans ; Intracellular Signaling Peptides and Proteins - cerebrospinal fluid ; Male ; Middle Aged ; Neuropeptides - cerebrospinal fluid ; Orexins ; Peptide Fragments - cerebrospinal fluid ; Polysomnography ; Severity of Illness Index ; Sleep Wake Disorders - cerebrospinal fluid ; Sleep Wake Disorders - etiology ; Sleep Wake Disorders - physiopathology ; tau Proteins - cerebrospinal fluid</subject><ispartof>JAMA neurology, 2014-12, Vol.71 (12), p.1498-1505</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a326t-4908178eefebb6061c019e96e5de2705033d75bea17724590e60b4e13ef3cc5b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://jamanetwork.com/journals/jamaneurology/articlepdf/10.1001/jamaneurol.2014.2510$$EPDF$$P50$$Gama$$H</linktopdf><linktohtml>$$Uhttps://jamanetwork.com/journals/jamaneurology/fullarticle/10.1001/jamaneurol.2014.2510$$EHTML$$P50$$Gama$$H</linktohtml><link.rule.ids>64,315,782,786,3344,27933,27934,76499,76502</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25322206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liguori, Claudio</creatorcontrib><creatorcontrib>Romigi, Andrea</creatorcontrib><creatorcontrib>Nuccetelli, Marzia</creatorcontrib><creatorcontrib>Zannino, Silvana</creatorcontrib><creatorcontrib>Sancesario, Giuseppe</creatorcontrib><creatorcontrib>Martorana, Alessandro</creatorcontrib><creatorcontrib>Albanese, Maria</creatorcontrib><creatorcontrib>Mercuri, Nicola Biagio</creatorcontrib><creatorcontrib>Izzi, Francesca</creatorcontrib><creatorcontrib>Bernardini, Sergio</creatorcontrib><creatorcontrib>Nitti, Alessandra</creatorcontrib><creatorcontrib>Sancesario, Giulia M</creatorcontrib><creatorcontrib>Sica, Francesco</creatorcontrib><creatorcontrib>Marciani, Maria G</creatorcontrib><creatorcontrib>Placidi, Fabio</creatorcontrib><title>Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease</title><title>JAMA neurology</title><addtitle>JAMA Neurol</addtitle><description>IMPORTANCE: Nocturnal sleep disruption develops in Alzheimer disease (AD) owing to the derangement of the sleep-wake cycle regulation pathways. Orexin contributes to the regulation of the sleep-wake cycle by increasing arousal levels and maintaining wakefulness. OBJECTIVES: To study cerebrospinal fluid levels of orexin in patients with AD, to evaluate the relationship of orexin cerebrospinal fluid levels with the degree of dementia and the cerebrospinal fluid AD biomarkers (tau proteins and β-amyloid 1-42), and to analyze potentially related sleep architecture changes measured by polysomnography. DESIGN, SETTING, AND PARTICIPANTS: We conducted a case-control study from August 1, 2012, through May 31, 2013. We included 48 drug-naive AD patients referred to the Neurological Clinic of the University Hospital of Rome Tor Vergata. Based on the Mini-Mental State Examination score, 21 patients were included in mild AD group (score, ≥21), whereas 27 were included in the moderate to severe AD group (score, <21). The control group consisted of 29 nondemented participants of similar age and sex. EXPOSURE: Laboratory assessment of cerebrospinal fluid levels of orexin, tau proteins, and β-amyloid 1-42 and polysomnographic assessment of sleep variables. MAIN OUTCOMES AND MEASURES: Levels of orexin, tau proteins, and β-amyloid 1-42; macrostructural variables of nocturnal sleep (total sleep time, sleep efficiency, sleep onset and rapid eye movement [REM] sleep latencies, non-REM and REM sleep stages, and wakefulness after sleep onset); and Mini-Mental State Examination scores. RESULTS: Patients with moderate to severe AD presented with higher mean (SD) orexin levels compared with controls (154.36 [28.16] vs 131.03 [26.55]; P < .01) and with more impaired nocturnal sleep with respect to controls and patients with mild AD. On the other hand, in the global AD group, orexin levels were positively correlated with total tau protein levels (r = 0.32; P = .03) and strictly related to sleep impairment. Finally, cognitive impairment, as measured by the Mini-Mental State Examination, was correlated with sleep structure deterioration. CONCLUSIONS AND RELEVANCE: Our results demonstrate that, in AD, increased cerebrospinal fluid orexin levels are related to a parallel sleep deterioration, which appears to be associated with cognitive decline. Therefore, the orexinergic system seems to be dysregulated in AD, and its output and function appear to be overexpressed along the progression of the neurodegenerative process. This overexpression may result from an imbalance of the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>Case-Control Studies</subject><subject>Cognition Disorders - cerebrospinal fluid</subject><subject>Cognition Disorders - etiology</subject><subject>Cognition Disorders - physiopathology</subject><subject>Female</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - cerebrospinal fluid</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neuropeptides - cerebrospinal fluid</subject><subject>Orexins</subject><subject>Peptide Fragments - cerebrospinal fluid</subject><subject>Polysomnography</subject><subject>Severity of Illness Index</subject><subject>Sleep Wake Disorders - cerebrospinal fluid</subject><subject>Sleep Wake Disorders - etiology</subject><subject>Sleep Wake Disorders - physiopathology</subject><subject>tau Proteins - cerebrospinal fluid</subject><issn>2168-6149</issn><issn>2168-6157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkM1PAjEQxRujEYL8A8aYHj2wOG233d0jAT9ISDigVzfdZcCS_cB214h_vSUgzGXm8N6bvB8hdwyGDIA9bnSpK2xtXQw5sHDIJYML0uVMxYFiMro83WHSIX3nNuAnBghFeE06XArOOagu-Zhb_DEV2rXJ6WLnGizpZOcsrttCN6auBnRRIG7ptNxqY0usmgHV1ZKO63VlGvONdIJ54ROoqeio-P1EU6KlE-NQO7whVytdOOwfd4-8Pz-9jV-D2fxlOh7NAi24aoIwgZhFMeIKs0yBYjmwBBOFcok8AglCLCOZoWZRxEOZACrIQmQCVyLPZSZ65OGQu7X1V4uuSUvjciwKT6luXcqUkL68VImXhgdpbmvni67SrTWltruUQbqHm57hpnu46R6ut90fP7RZicuT6R-lF9weBN59jkyYlDEXf6AwgIg</recordid><startdate>20141201</startdate><enddate>20141201</enddate><creator>Liguori, Claudio</creator><creator>Romigi, Andrea</creator><creator>Nuccetelli, Marzia</creator><creator>Zannino, Silvana</creator><creator>Sancesario, Giuseppe</creator><creator>Martorana, Alessandro</creator><creator>Albanese, Maria</creator><creator>Mercuri, Nicola Biagio</creator><creator>Izzi, Francesca</creator><creator>Bernardini, Sergio</creator><creator>Nitti, Alessandra</creator><creator>Sancesario, Giulia M</creator><creator>Sica, Francesco</creator><creator>Marciani, Maria G</creator><creator>Placidi, Fabio</creator><general>American Medical Association</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20141201</creationdate><title>Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease</title><author>Liguori, Claudio ; Romigi, Andrea ; Nuccetelli, Marzia ; Zannino, Silvana ; Sancesario, Giuseppe ; Martorana, Alessandro ; Albanese, Maria ; Mercuri, Nicola Biagio ; Izzi, Francesca ; Bernardini, Sergio ; Nitti, Alessandra ; Sancesario, Giulia M ; Sica, Francesco ; Marciani, Maria G ; Placidi, Fabio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a326t-4908178eefebb6061c019e96e5de2705033d75bea17724590e60b4e13ef3cc5b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - cerebrospinal fluid</topic><topic>Alzheimer Disease - complications</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Amyloid beta-Peptides - cerebrospinal fluid</topic><topic>Case-Control Studies</topic><topic>Cognition Disorders - cerebrospinal fluid</topic><topic>Cognition Disorders - etiology</topic><topic>Cognition Disorders - physiopathology</topic><topic>Female</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - cerebrospinal fluid</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neuropeptides - cerebrospinal fluid</topic><topic>Orexins</topic><topic>Peptide Fragments - cerebrospinal fluid</topic><topic>Polysomnography</topic><topic>Severity of Illness Index</topic><topic>Sleep Wake Disorders - cerebrospinal fluid</topic><topic>Sleep Wake Disorders - etiology</topic><topic>Sleep Wake Disorders - physiopathology</topic><topic>tau Proteins - cerebrospinal fluid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liguori, Claudio</creatorcontrib><creatorcontrib>Romigi, Andrea</creatorcontrib><creatorcontrib>Nuccetelli, Marzia</creatorcontrib><creatorcontrib>Zannino, Silvana</creatorcontrib><creatorcontrib>Sancesario, Giuseppe</creatorcontrib><creatorcontrib>Martorana, Alessandro</creatorcontrib><creatorcontrib>Albanese, Maria</creatorcontrib><creatorcontrib>Mercuri, Nicola Biagio</creatorcontrib><creatorcontrib>Izzi, Francesca</creatorcontrib><creatorcontrib>Bernardini, Sergio</creatorcontrib><creatorcontrib>Nitti, Alessandra</creatorcontrib><creatorcontrib>Sancesario, Giulia M</creatorcontrib><creatorcontrib>Sica, Francesco</creatorcontrib><creatorcontrib>Marciani, Maria G</creatorcontrib><creatorcontrib>Placidi, Fabio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>JAMA neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liguori, Claudio</au><au>Romigi, Andrea</au><au>Nuccetelli, Marzia</au><au>Zannino, Silvana</au><au>Sancesario, Giuseppe</au><au>Martorana, Alessandro</au><au>Albanese, Maria</au><au>Mercuri, Nicola Biagio</au><au>Izzi, Francesca</au><au>Bernardini, Sergio</au><au>Nitti, Alessandra</au><au>Sancesario, Giulia M</au><au>Sica, Francesco</au><au>Marciani, Maria G</au><au>Placidi, Fabio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease</atitle><jtitle>JAMA neurology</jtitle><addtitle>JAMA Neurol</addtitle><date>2014-12-01</date><risdate>2014</risdate><volume>71</volume><issue>12</issue><spage>1498</spage><epage>1505</epage><pages>1498-1505</pages><issn>2168-6149</issn><eissn>2168-6157</eissn><abstract>IMPORTANCE: Nocturnal sleep disruption develops in Alzheimer disease (AD) owing to the derangement of the sleep-wake cycle regulation pathways. Orexin contributes to the regulation of the sleep-wake cycle by increasing arousal levels and maintaining wakefulness. OBJECTIVES: To study cerebrospinal fluid levels of orexin in patients with AD, to evaluate the relationship of orexin cerebrospinal fluid levels with the degree of dementia and the cerebrospinal fluid AD biomarkers (tau proteins and β-amyloid 1-42), and to analyze potentially related sleep architecture changes measured by polysomnography. DESIGN, SETTING, AND PARTICIPANTS: We conducted a case-control study from August 1, 2012, through May 31, 2013. We included 48 drug-naive AD patients referred to the Neurological Clinic of the University Hospital of Rome Tor Vergata. Based on the Mini-Mental State Examination score, 21 patients were included in mild AD group (score, ≥21), whereas 27 were included in the moderate to severe AD group (score, <21). The control group consisted of 29 nondemented participants of similar age and sex. EXPOSURE: Laboratory assessment of cerebrospinal fluid levels of orexin, tau proteins, and β-amyloid 1-42 and polysomnographic assessment of sleep variables. MAIN OUTCOMES AND MEASURES: Levels of orexin, tau proteins, and β-amyloid 1-42; macrostructural variables of nocturnal sleep (total sleep time, sleep efficiency, sleep onset and rapid eye movement [REM] sleep latencies, non-REM and REM sleep stages, and wakefulness after sleep onset); and Mini-Mental State Examination scores. RESULTS: Patients with moderate to severe AD presented with higher mean (SD) orexin levels compared with controls (154.36 [28.16] vs 131.03 [26.55]; P < .01) and with more impaired nocturnal sleep with respect to controls and patients with mild AD. On the other hand, in the global AD group, orexin levels were positively correlated with total tau protein levels (r = 0.32; P = .03) and strictly related to sleep impairment. Finally, cognitive impairment, as measured by the Mini-Mental State Examination, was correlated with sleep structure deterioration. CONCLUSIONS AND RELEVANCE: Our results demonstrate that, in AD, increased cerebrospinal fluid orexin levels are related to a parallel sleep deterioration, which appears to be associated with cognitive decline. Therefore, the orexinergic system seems to be dysregulated in AD, and its output and function appear to be overexpressed along the progression of the neurodegenerative process. This overexpression may result from an imbalance of the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.</abstract><cop>United States</cop><pub>American Medical Association</pub><pmid>25322206</pmid><doi>10.1001/jamaneurol.2014.2510</doi><tpages>8</tpages></addata></record> |
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| ispartof | JAMA neurology, 2014-12, Vol.71 (12), p.1498-1505 |
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| subjects | Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - complications Alzheimer Disease - physiopathology Amyloid beta-Peptides - cerebrospinal fluid Case-Control Studies Cognition Disorders - cerebrospinal fluid Cognition Disorders - etiology Cognition Disorders - physiopathology Female Humans Intracellular Signaling Peptides and Proteins - cerebrospinal fluid Male Middle Aged Neuropeptides - cerebrospinal fluid Orexins Peptide Fragments - cerebrospinal fluid Polysomnography Severity of Illness Index Sleep Wake Disorders - cerebrospinal fluid Sleep Wake Disorders - etiology Sleep Wake Disorders - physiopathology tau Proteins - cerebrospinal fluid |
| title | Orexinergic System Dysregulation, Sleep Impairment, and Cognitive Decline in Alzheimer Disease |
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