Although amyloid-β protein is the core pathologic feature of Alzheimer's disease, biomarkers of neuronal degeneration are the only ones believed to provide satisfactory predictions of clinical progression within short time frames.
MAZ is an inflammation-responsive transcription factor that has been co-localized to pathologic structures in Alzheimer's disease brain while up regulation of E2F1 has been shown to trigger cell cycle re-entry of post-mitotic neurons leading to the initiation of apoptosis in neurodegeneration associated with Parkinson's disease [38], [39].
We have utilized 2DE to begin characterization of the complex pathologic processes in Alzheimer's disease (AD).
Matrix metalloproteinases (MMP) are believed to be involved in the pathologic processes behind Alzheimer's disease (AD).
Moreover, insulin resistance, high insulin levels, and cholesterol are all implicated in β-amyloid accumulation in the brain the pathologic hallmark of Alzheimer's disease (22).
The definitive pathologic hallmarks of Alzheimer's disease, the presence of amyloid plaques and neurofibrillary tangles, can only be detected currently by examining the brain at postmortem.
The oligomer cascade hypothesis, which states that oligomers are the initiating pathologic agents in Alzheimer's disease, has all but supplanted the amyloid cascade hypothesis, which suggested that fibers were the key etiologic agents in Alzheimer's disease.
In the past decade, positron emission tomography (PET) with carbon-11-labeled Pittsburgh Compound B (PIB) has revolutionized the neuroimaging of aging and dementia by enabling in vivo detection of amyloid plaques, a core pathologic feature of Alzheimer's disease (AD).
Positron emission tomography (PET) with amyloid ligands has revolutionized neuroimaging of aging and dementia in the past decade by enabling the detection and quantification of amyloid plaques, a core pathologic feature of Alzheimer's disease (AD) [ 1].
The purpose of this study was to use serial PIB and magnetic resonance imaging to gain insight into the sequence of pathologic events in Alzheimer's disease, and the clinical features associated with this sequence.
