[¹⁸F]FDG-PET in Patients with Alzheimer’s Disease: Marker of Disease Spread

Abstract

Background: It is not known yet whether temporoparietal glucose hypometabolism in patients with probable Alzheimer’s disease (AD) reflects disease severity or different subtypes of patients. Methods: Twenty-five subjects with mild probable AD [NINCDS-ADRDA criteria; age 65.8 ± 9.3 years (mean ± SD); Mini-Mental State Examination (MMSE) 26.0 ± 3.3] were investigated. [¹⁸F]FDG-PET data were analyzed visually with raters blinded to the diagnosis and with a quantitative analysis in the region of interest on individual anatomically normalized PET scans. Results: Thirteen of 25 patients showed temporoparietal hypometabolism on visual inspection (PET+; age 65.7 ± 10.7), 12 patients had normal FDG-PET results (PET–; age 65.9 ± 8.0; n.s.). The MMSE and immediate reproduction of the Wechsler Memory Scale (WMS-R-I) were 27.7 ± 1.9 and 31.1 ± 6.1 in the PET– vs. 24.5 ± 3.6 (p = 0.012) and 22.0 ± 7.4 (p = 0.006) in the PET+ group. Immediate and delayed recall in the California Verbal Learning Test and delayed reproduction in the Wechsler Memory Scale were alike. Regression analysis revealed a significant correlation of temporoparietal glucose metabolism with the block span (r = 0.60; p < 0.01) and the WMS-R-I (r = 0.68; p < 0.01) but not with measures of hippocampal function. Conclusions: Temporoparietal glucose metabolism in patients with very mild AD is a sign of disease spread beyond the temporal lobe. This may aid in establishing objective parameters for future therapeutic studies.

Relationships between hippocampal microstructure, metabolism, and function in early Alzheimer’s disease

“…Together with methodological issues (Mevel et al 2007), this phenomenon, i.e., a variable extent and efficacy of AD-related synaptic reorganisation in the hippocampus (Masliah et al 2006), may well account for the inconsistent findings in respect of the association between hippocampal metabolism and episodic memory (see ''Introduction''). Accordingly, and in line with the numerous reports (e.g., Bittner et al 2005;Kalpouzos et al 2005;Salmon et al 2008), we did not observe a strong relationship between hippocampal metabolism and memory performance in our subjects with early AD. Considering a modest sample size, however, this finding should be considered with caution.…”

Domain-Specific Improvement of Cognition on Memantine in Patients with Alzheimer’s Disease Treated with Rivastigmine

“…With sophisticated methods such as functional magnetic resonance imaging, this impairment of hippocampal function may be portrayed objectively [34] and was shown to reflect a continuum from health to disease [35] . With progressing disease, AD subsequently affects the parietal and frontal lobe [31] , which may also be portrayed objectively with elaborated and expensive methods [36] . In functional terms, the spread of AD results in deficits of spatial orientation, attention and executive functions as well as working memory and language [33] .…”

The Neurofilament Heavy Chain (NfH^SMI35) in the Cerebrospinal Fluid Diagnosis of Alzheimer’s Disease

“…CSF was aliquoted, immediately frozen and stored at -80 ° C until analysis. Neuropsychological testing was performed on a single day with a previously described test battery [21,22] , including the Mini-Mental State Examination (MMSE) as a general screening test [23] . The control group consisted of 58 nondemented patients age-matched to AD, including 34 patients who presented with tension-type headache and showed no evidence of a structural, hemorrhagic or infl ammatory lesion as well as 24 patients fulfi lling the criteria of a major depressive disorder [17] .…”