Abstract
BackgroundAbnormal orexin-A levels in cerebrospinal fluid (CSF) have been identified in Alzheimer’s disease (AD) and other neurodegenerative diseases. However, few studies have focused on Lewy body disease (LBD) and often with debatable outcomes. Thus, we performed this systematic review and meta-analysis to investigate orexin-A levels in LBD by incorporating data from different studies.MethodsWe gathered studies comparing orexin-A levels in patients with LBD and controls (including healthy controls and other dementia subtypes). In the initial search, 117 relevant articles were identified. After a selection process, seven studies, conducted in Japan, USA, Spain, Switzerland, France, Italy, and Netherlands, were chosen.ResultsIn total, 179 patients with LBD and 253 controls were included. Patients with LBD had significantly lower mean orexin-A CSF levels when compared with patients with AD [standard mean difference (SMD): −0.35, 95% confidence interval (CI): −0.70 to −0.00, Z = 1.96, P = 0.05], whereas mean orexin-A levels were significantly higher when compared with patients with frontotemporal lobar degeneration (FTLD) (SMD: 0.61, 95% CI: 0.23–0.99, Z = 3.12, P = 0.002). Orexin-A CSF levels in LBD patients were approximately equal to levels in healthy elderly individuals, whereas they were significantly decreased in LBD patients with excessive daytime sleepiness (EDS) (SMD: -0.15, 95% CI: -0.59 to 0.29, Z = 0.67, P = 0.50).ConclusionsWe showed that orexin-A levels in patients with LBD were not very different from those in normal elderly individuals, whereas they were lower than those in AD patients and higher than those in FTLD patients. The influence of hypersomnia on orexin-A levels should be carefully interpreted.Systematic Review Registration https://www.crd.york.ac.uk/prospero/, identifier CRD42021265900.
Highlights
Lewy body disease (LBD) is characterized by the presence of Lewy bodies (LBs) and Lewy neurites, with senile plaque (SP) and neurofibrillary tangle (NFT) deposition [1]
Patients with LBD had significantly lower mean orexin-A cerebrospinal fluid (CSF) levels when compared with patients with Alzheimer’s disease (AD) [standard mean difference (SMD): −0.35, 95% confidence interval (CI): −0.70 to −0.00, Z = 1.96, P = 0.05], whereas mean orexin-A levels were significantly higher when compared with patients with frontotemporal lobar degeneration (FTLD) (SMD: 0.61, 95% CI: 0.23–0.99, Z = 3.12, P = 0.002)
Orexin-A CSF levels in LBD patients were approximately equal to levels in healthy elderly individuals, whereas they were significantly decreased in LBD patients with excessive daytime sleepiness (EDS) (SMD: -0.15, 95% CI: -0.59 to 0.29, Z = 0.67, P = 0.50)
Summary
Lewy body disease (LBD) is characterized by the presence of Lewy bodies (LBs) and Lewy neurites, with senile plaque (SP) and neurofibrillary tangle (NFT) deposition [1]. LBD comprises a diagnostic spectrum that includes Parkinson’s disease (PD), PD with dementia (PDD), and dementia with Lewy bodies (DLB). DLB and PDD are differentiated based on the “oneyear rule,” which accounts for the relationship between parkinsonism symptoms and dementia. The hypothalamic neurotransmitter, orexin-A (hypocretin-1), is believed to play a crucial role in the orexinergic system; it contributes to the regulation of the sleep– wake cycle by increasing arousal levels and maintaining wakefulness and maintaining memory and spatial cognition functions [3, 4]. Orexin-A interacts with multiple areas in the brain stem and other neurotransmitter systems, including dopamine [5]. Few studies have focused on Lewy body disease (LBD) and often with debatable outcomes. We performed this systematic review and meta-analysis to investigate orexin-A levels in LBD by incorporating data from different studies
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