[ ¹¹ C]PIB in a nondemented population

Abstract

Elevated [(11)C]PIB binding in nondemented subjects suggests that [(11)C]PIB amyloid imaging may be sensitive for detection of a preclinical Alzheimer disease state. Longitudinal studies will be required to determine the association of elevated [(11)C]PIB binding and risk of developing dementia of the Alzheimer type.

Functional brain network centrality is related to APOE genotype in cognitively normal elderly

“…The plots per subgroup show that EC variability against test score is lower in e4 carriers. This indicates differences in brain network organization between carriers and noncarriers that make the brain more vulnerable to AD‐related pathology (De Meyer et al., 2010; Evans et al., 2014; Mintun et al., 2006; Sperling et al., 2011). In an important way, this does not lead to decreased cognitive decline or visuoperceptual performance.…”

Cortical phase changes in Alzheimer's disease at 7T MRI: A novel imaging marker

“…Table 2 Mean phase shifts and standard deviations (SD) of the cortical and hippocampal subregions in AD patients and control subjects plaques but is also affected at a later stage of AD than the neocortex [41][42][43]. This sequence of events has been confirmed by PiB-PET studies showing high amyloid loads in the parietal and frontal lobes and not in hippocampus [5][6][7]44,45]. However, phase shift changes might be caused by other factors than iron-bound plaques, such as iron itself or iron-bound CAA, but also by geometry and orientation.…”

“…Mormino and colleagues [48] showed high sensitivity (90%) and specificity (90%) in differentiating AD patients from control subjects. However, within the group of healthy subjects, the specificity drops with increasing age, because the percentage of positive PiB-PET scans increases rapidly, with 12% of the people in their 60s, 30% in their 70s, and 50% in their 80s giving false-positive results [45,49,50]. Our data show that measurement of phase shift using T2*-weighted MRI might improve the specificity of AD diagnosis.…”

Impact of amyloid imaging on drug development in Alzheimer's disease

“…Aβ deposition is believed to begin in normal elderly subjects, who subsequently may develop signs of mild cognitive impairment (MCI), and then may finally develop AD (Figs 3 and 4), in whom post mortem analysis demonstrates the characteristic abundance of Aβ plaques in specific brain areas. Recent PET studies using [ 11 C]PiB in elderly normal control subjects support the existence of a preclinical AD stage in which Aβ plaques are found in discrete brain regions by demonstrating the presence of significant radioligand retention, approaching levels seen in AD subjects, in about 10% of the elderly control subjects [14]. In addition, Aβ plaques are often found in Parkinson's disease subjects with co-morbid dementia and in diffuse Lewy body (DLB) disease patients [15].…”

“…Thus from an AD diagnostic perspective, one would look for the presence of Aβ deposits or the binding of an Aβ imaging agent in specific brain regions, and the absence of binding in other regions. However, the presence of significant Aβ deposits in specific brain regions does not necessarily indicate the presence or severity of clinical AD, as some control and MCI subjects contain concentrations of Aβ plaques in their brains as high as contained in the brains of AD subjects (Fig 5) [14,22,23]. The coincidence of high Aβ loads and the absence or lack of extensive cognitive deficits in some subjects could be interpreted as high resistance to Aβ damage (i.e., a high cognitive reserve) or could indicate that excessive Aβ has not been present for a sufficiently long time in some subjects to cause as much damage as in AD subjects.…”