Meta-analysis of cerebrospinal fluid neuron-specific enolase levels in Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. 2021

Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
Department of Neurology, Asahikawa City Hospital, 1-1-65 Kinseicho, Asahikawa, 070-8610, Japan. katataka@gmail.com.

This study examined the usefulness of cerebrospinal fluid (CSF) neuron-specific enolase (NSE) levels as a candidate biomarker of neurodegeneration in Alzheimer's disease (AD), Parkinson's disease (PD), PD with dementia (PDD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). We performed a systematic search of PubMed, the Cochrane Library, Scopus, and Google Scholar to find studies that measured CSF NSE levels in AD, PD, DLB, and/or MSA. For each disease, we pooled all available data and performed a meta-analysis, and meta-regression analyses of age and sex were conducted if the main analysis found a significant association. Twenty studies were included (13 for AD, 8 for PD/PDD/DLB, and 4 for MSA). Significantly elevated CSF NSE levels were detected in AD (Hedges' g = 0.822, 95% confidence interval [95% CI] 0.332 to 1.311, p = 0.0010), but the data exhibited high heterogeneity (I2 = 88.43%, p < 0.001). The meta-regression analysis of AD showed that age (p < 0.001), but not sex, had a significant effect on CSF NSE levels. A meta-analysis of the pooled data for PD/PDD/DLB did not show any significant changes in the CSF NSE level, but a sub-group analysis of PDD/DLB revealed significantly elevated CSF NSE levels (Hedges' g = 0.507, 95% CI 0.020 to 0.993, p = 0.0412). No significant changes in CSF NSE levels were detected in MSA. The CSF NSE level may be a useful biomarker of neurodegeneration in AD and PDD/DLB. Age was found to affect the CSF NSE levels of AD patients.

UI MeSH Term Description Entries
D010300 Parkinson Disease A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75) Idiopathic Parkinson Disease,Lewy Body Parkinson Disease,Paralysis Agitans,Primary Parkinsonism,Idiopathic Parkinson's Disease,Lewy Body Parkinson's Disease,Parkinson Disease, Idiopathic,Parkinson's Disease,Parkinson's Disease, Idiopathic,Parkinson's Disease, Lewy Body,Parkinsonism, Primary
D010751 Phosphopyruvate Hydratase A hydro-lyase that catalyzes the dehydration of 2-phosphoglycerate to form PHOSPHOENOLPYRUVATE. Several different isoforms of this enzyme exist, each with its own tissue specificity. Enolase,Neuron-Specific Enolase,2-Phospho-D-Glycerate Hydro-Lyase,2-Phospho-D-Glycerate Hydrolase,2-Phosphoglycerate Dehydratase,Enolase 2,Enolase 3,Muscle-Specific Enolase,Nervous System-Specific Enolase,Non-Neuronal Enolase,alpha-Enolase,beta-Enolase,gamma-Enolase,2 Phospho D Glycerate Hydro Lyase,2 Phospho D Glycerate Hydrolase,2 Phosphoglycerate Dehydratase,Dehydratase, 2-Phosphoglycerate,Enolase, Muscle-Specific,Enolase, Nervous System-Specific,Enolase, Neuron-Specific,Enolase, Non-Neuronal,Hydratase, Phosphopyruvate,Hydro-Lyase, 2-Phospho-D-Glycerate,Muscle Specific Enolase,Nervous System Specific Enolase,Neuron Specific Enolase,Non Neuronal Enolase,System-Specific Enolase, Nervous,alpha Enolase,beta Enolase,gamma Enolase
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000544 Alzheimer Disease A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57) Acute Confusional Senile Dementia,Alzheimer's Diseases,Dementia, Alzheimer Type,Dementia, Senile,Presenile Alzheimer Dementia,Senile Dementia, Alzheimer Type,Alzheimer Dementia,Alzheimer Disease, Early Onset,Alzheimer Disease, Late Onset,Alzheimer Sclerosis,Alzheimer Syndrome,Alzheimer Type Senile Dementia,Alzheimer's Disease,Alzheimer's Disease, Focal Onset,Alzheimer-Type Dementia (ATD),Dementia, Presenile,Dementia, Primary Senile Degenerative,Early Onset Alzheimer Disease,Familial Alzheimer Disease (FAD),Focal Onset Alzheimer's Disease,Late Onset Alzheimer Disease,Primary Senile Degenerative Dementia,Senile Dementia, Acute Confusional,Alzheimer Dementias,Alzheimer Disease, Familial (FAD),Alzheimer Diseases,Alzheimer Type Dementia,Alzheimer Type Dementia (ATD),Alzheimers Diseases,Dementia, Alzheimer,Dementia, Alzheimer-Type (ATD),Familial Alzheimer Diseases (FAD),Presenile Dementia,Sclerosis, Alzheimer,Senile Dementia
D019578 Multiple System Atrophy A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92) Multiple System Atrophy Syndrome,Multisystem Atrophy,Multisystemic Atrophy,Atrophies, Multisystem,Atrophies, Multisystemic,Atrophy, Multiple System,Atrophy, Multisystem,Atrophy, Multisystemic,Multiple System Atrophies,Multisystem Atrophies,Multisystemic Atrophies
D020961 Lewy Body Disease A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124) Dementia, Lewy Body,Diffuse Lewy Body Disease,Cortical Lewy Body Disease,Lewy Body Dementia,Lewy Body Disease, Cortical,Lewy Body Disease, Diffuse,Lewy Body Type Senile Dementia

Related Publications

Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
January 1995, Neuroscience letters,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
December 1999, Rinsho shinkeigaku = Clinical neurology,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
November 2008, Biological psychiatry,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
June 2014, Neuroscience letters,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
December 1999, Parkinsonism & related disorders,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
January 2001, Methods in molecular medicine,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
January 2000, Annals of the New York Academy of Sciences,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
January 1994, Journal of neural transmission. Parkinson's disease and dementia section,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
January 2014, Alzheimer's research & therapy,
Takayuki Katayama, and Jun Sawada, and Kae Takahashi, and Osamu Yahara, and Naoyuki Hasebe
July 2015, Movement disorders : official journal of the Movement Disorder Society,
Copied contents to your clipboard!