Department of Medical Imaging, Radboud University Medical Center, Geert Grooteplein Zuid 10, Nijmegen, 6525 EZ, The Netherlands.
Department of Medical Imaging, Jeroen Bosch Hospital, 's Hertogenbosch, The Netherlands.
Alzheimers Res Ther. 2024 Oct 29;16(1):241. doi: 10.1186/s13195-024-01604-7.
The loss of olfactory function is known to occur in patients suffering from (behavioral variant) frontotemporal dementia ((bv)FTD) and Alzheimer's disease (AD), although different pathophysiological mechanisms underpin this clinical symptom in both disorders. This study assessed whether brain metabolism of the olfactory circuit as assessed by positron emission tomography (PET) imaging with 2-[fluorine-18]fluoro-2-deoxy-d-glucose ([F]-FDG) can distinguish these entities in different subsets of patients.
Patients presenting with cognitive decline were included from a prospectively kept database: (1) bvFTD patients, (2) AD patients and (3) patients with logopenic primary progressive aphasia (PPA). Metabolic rates were calculated for different regions of the olfactory circuit for each subgroup and compared with a cohort of subjects with normal brain metabolism. Additionally, in patients with a logopenic PPA pattern on PET-imaging, statistical parametric mapping (SPM) analysis was performed.
The metabolism of subdivisions of the olfactory circuit as assessed by [F]-FDG PET brain imaging to bvFTD and AD from control subjects resulted in sensitivity/specificity rates of 95/87.5% and 80/83.3%, respectively. A sensitivity/specificity rate of 100/87.5% was achieved when used to differentiate AD from bvFTD. In patients with the PPA pattern on imaging, the underlying cause (either FTD or AD) could be determined with a sensitivity/specificity rate of 88/82%. SPM analysis concurred that different regions of the olfactory circuit were affected in patients suffering from AD PPA or bvFTD PPA.
Metabolic dysfunction in the olfactory circuit is different in various neurodegenerative disorders. Further investigation of the correlations between the cerebral metabolism and the mechanisms which drive olfactory dysfunction is needed.
已知嗅觉功能丧失发生在患有（行为变异）额颞叶痴呆（bvFTD）和阿尔茨海默病（AD）的患者中，尽管这两种疾病的这种临床症状有不同的病理生理学机制。本研究评估了正电子发射断层扫描（PET）成像用 2-[氟-18]氟-2-脱氧-d-葡萄糖（[F]-FDG）评估的嗅觉回路的脑代谢是否可以区分这些实体在不同的患者亚组中。
从一个前瞻性保存的数据库中纳入表现出认知能力下降的患者：（1）bvFTD 患者，（2）AD 患者和（3）失语法性原发性进行性失语症（PPA）患者。为每个亚组的嗅觉回路的不同区域计算代谢率，并与具有正常脑代谢的受试者队列进行比较。此外，在 PET 成像上具有失语法性 PPA 模式的患者中，进行了统计参数映射（SPM）分析。
使用 [F]-FDG PET 脑成像评估嗅觉回路的细分，对 bvFTD 和 AD 与对照患者的结果得出的敏感性/特异性率分别为 95/87.5%和 80/83.3%。当用于区分 AD 与 bvFTD 时，可达到 100/87.5%的敏感性/特异性率。在成像上具有 PPA 模式的患者中，潜在病因（FTD 或 AD）的确定具有 88/82%的敏感性/特异性率。SPM 分析一致认为，在患有 AD PPA 或 bvFTD PPA 的患者中，嗅觉回路的不同区域受到影响。
在各种神经退行性疾病中，嗅觉回路的代谢功能障碍不同。需要进一步研究大脑代谢与驱动嗅觉功能障碍的机制之间的相关性。
