Molecular Imaging of Alzheimer Disease Pathology

Abstract

Development of molecular imaging agents for fibrillar β–amyloid (Aβ) positron emission tomography (PET) during the last decade brought molecular imaging of Alzheimer’s disease (AD) pathology into the spotlight. Large cohort studies with longitudinal follow-up in cognitively normal, mild cognitive impairment and AD patients indicate that Aβ deposition can be detected many years before the onset of symptoms with molecular imaging and its progression can be followed longitudinally. The utility of Aβ PET in differential diagnosis of AD is greatest when there is no pathologic overlap between the two dementia syndromes such as in frontotemporal lobar degeneration and AD. However Aβ PET alone may be insufficient in distinguishing dementia syndromes that commonly have overlapping Aβ pathology, such as dementia with Lewy bodies and vascular dementia, which represent the two most common dementia pathologies after AD. The role of molecular imaging in AD clinical trials is growing rapidly especially in an era when preventive interventions are designed towards eradicating the pathology targeted by molecular imaging agents.

Role of Toll-like receptor/MYD88 signaling in neurodegenerative diseases

“…AD can lead to cognitive decline, memory loss, language problems, and the deterioration of executive function. The inflammatory response to the extracellular A β -containing plaques is central to this disease ( Kantarci, 2014 ;Morales et al, 2014 ;Sorrentino et al, 2014 ). Microglia play a key role in the inflammation response and are usually found around senile plaques in the brains of AD patients.…”

Brain PET in the Diagnosis of Alzheimer’s Disease

“…The PET imaging tracers help in differentiating dementia syndromes, which do not have overlap of the underlying pathological process. 13 The purpose of this article was to review the role of brain PET imaging in the diagnosis of AD.…”

Review of ‘the Potential Role of Arterial Stiffness in the Pathogenesis of Alzheimer’s Disease’

“…The use of Aβ-specific ligands in PET has opened new avenues for AD pathology research (reviewed by Kantarchi [67] ). Arguably one of the most important contributions of Aβ-PET imaging in recent years was empirical evidence that brain Aβ-deposition does not reside solely in the domain of AD pathology, but is also a component of brain aging [68,69] .…”

“…Extensive Aβ deposition precedes cognitive impairment, and is associated with APOE genotype, age and a higher risk of cognitive decline [78] . Population-based studies with Aβ-PET shows the prevalence of AD-like Aβ deposition is between 20 and 34% in cognitively normal older adults [67] and increases dramatically with increasing age [15,69] . Recently, we showed that 9th decade of life the proportion of nondemented older adults with AD-like Aβ deposition increased from 45 to 75% over 2 years of follow-up [13] .…”