PDF(Pubmed)
Abstract：
OBJECTIVE: Does neurodegenerative disease underlie the increased rate of dementia observed in older people with schizophrenia? Several studies have reported a higher prevalence of dementia in people with schizophrenia compared with the general population. This may reflect a higher risk of developing neurodegenerative diseases such as vascular dementia or Alzheimer\'s disease (AD). Alternatively, this may reflect non-pathological, age-related cognitive decline in a population with low cognitive reserve.
METHODS: We reviewed papers that compared postmortem findings, hippocampal MRI volume or cerebrospinal fluid (CSF) markers of AD, between patients with schizophrenia with evidence of cognitive impairment (age ≥45 years) with controls. We subsequently performed a meta-analysis of postmortem studies that compared amyloid-β plaques (APs) or neurofibrillary tangles (NFTs) in cognitively impaired patients with schizophrenia to normal controls or an AD group.
RESULTS: No studies found a significant increase of APs or NFTs in cognitively impaired patients with schizophrenia compared with controls. All postmortem studies that compared APs or NFTs in patients with schizophrenia to an AD group found significantly more APs or NFTs in AD. No studies found a significant differences in CSF total tau or phosphorylated tau between patients with schizophrenia and controls. The two studies which compared CSF Aβ42 between patients with schizophrenia and controls found significantly decreased CSF Aβ42 in schizophrenia compared with controls. Hippocampal volume findings were mixed.
CONCLUSIONS: Studies have not found higher rates of AD-related pathology in cognitively impaired individuals with schizophrenia compared with controls. Higher rates of dementia identified in population studies may reflect a lack of specificity in clinical diagnostic tools used to diagnose dementia.
METHODS: We reviewed papers that compared postmortem findings, hippocampal MRI volume or cerebrospinal fluid (CSF) markers of AD, between patients with schizophrenia with evidence of cognitive impairment (age ≥45 years) with controls. We subsequently performed a meta-analysis of postmortem studies that compared amyloid-β plaques (APs) or neurofibrillary tangles (NFTs) in cognitively impaired patients with schizophrenia to normal controls or an AD group.
RESULTS: No studies found a significant increase of APs or NFTs in cognitively impaired patients with schizophrenia compared with controls. All postmortem studies that compared APs or NFTs in patients with schizophrenia to an AD group found significantly more APs or NFTs in AD. No studies found a significant differences in CSF total tau or phosphorylated tau between patients with schizophrenia and controls. The two studies which compared CSF Aβ42 between patients with schizophrenia and controls found significantly decreased CSF Aβ42 in schizophrenia compared with controls. Hippocampal volume findings were mixed.
CONCLUSIONS: Studies have not found higher rates of AD-related pathology in cognitively impaired individuals with schizophrenia compared with controls. Higher rates of dementia identified in population studies may reflect a lack of specificity in clinical diagnostic tools used to diagnose dementia.
摘要：
目的：在老年精神分裂症患者中，神经退行性疾病是痴呆发病率增加的原因吗？一些研究报道，与普通人群相比，精神分裂症患者痴呆的患病率更高。这可能反映出发生神经退行性疾病如血管性痴呆或阿尔茨海默病(AD)的风险较高。或者，这可能反映了非病态，认知储备低的人群与年龄相关的认知能力下降。
方法：我们回顾了比较死后发现的论文，AD的海马MRI体积或脑脊液（CSF）标记，有认知障碍证据的精神分裂症患者（年龄≥45岁）与对照组之间的关系。随后，我们对死后研究进行了荟萃分析，比较了认知障碍精神分裂症患者与正常对照组或AD组的淀粉样β斑块（AP）或神经原纤维缠结（NFT）。
结果：没有研究发现与对照组相比，认知受损的精神分裂症患者的AP或NFT显著增加。所有将精神分裂症患者的AP或NFT与AD组进行比较的验尸研究发现，AD中的AP或NFT明显更多。没有研究发现精神分裂症患者和对照组之间的CSF总tau或磷酸化tau存在显着差异。两项比较精神分裂症患者和对照组之间CSFAβ42的研究发现，与对照组相比，精神分裂症患者的CSFAβ42显着降低。海马体积的发现是混合的。
结论：研究未发现认知受损的精神分裂症患者的AD相关病理发生率高于对照组。在人群研究中发现的痴呆发生率较高可能反映了用于诊断痴呆的临床诊断工具缺乏特异性。
方法：我们回顾了比较死后发现的论文，AD的海马MRI体积或脑脊液（CSF）标记，有认知障碍证据的精神分裂症患者（年龄≥45岁）与对照组之间的关系。随后，我们对死后研究进行了荟萃分析，比较了认知障碍精神分裂症患者与正常对照组或AD组的淀粉样β斑块（AP）或神经原纤维缠结（NFT）。
结果：没有研究发现与对照组相比，认知受损的精神分裂症患者的AP或NFT显著增加。所有将精神分裂症患者的AP或NFT与AD组进行比较的验尸研究发现，AD中的AP或NFT明显更多。没有研究发现精神分裂症患者和对照组之间的CSF总tau或磷酸化tau存在显着差异。两项比较精神分裂症患者和对照组之间CSFAβ42的研究发现，与对照组相比，精神分裂症患者的CSFAβ42显着降低。海马体积的发现是混合的。
结论：研究未发现认知受损的精神分裂症患者的AD相关病理发生率高于对照组。在人群研究中发现的痴呆发生率较高可能反映了用于诊断痴呆的临床诊断工具缺乏特异性。
