Mark R. Emmerling

TL;DR: By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

TL;DR: It is likely that the water-soluble Aβ peptides the authors quantified are precursors to its insoluble, filamentous form, and reducing the levels of soluble Aβ in AD brains could have profound effects on AD pathophysiology.

TL;DR: The pathogenic effects of the dimeric Aβ-(1-40/42) were tested in cultures of rat hippocampal neuron glia cells and only in the presence of microglia did the dimer elicit neuronal killing.

TL;DR: The amounts of amyloid beta peptides in the central nervous system (CNS) and in reservoirs outside the CNS and their potential impact on Aβ plasma levels and Alzheimer's disease (AD) pathology are evaluated.

TL;DR: Sera obtained in the immediate postmortem from 100 individuals, 64 neuropathologically diagnosed Alzheimer's disease cases and 36 nondemented controls, were analyzed for cholesterol, lipoproteins, apolipoproteins (Apo), and triglycerides, suggesting for the first time that elevated cholesterol, especially in the form of LDL, influences the expression of AD-related pathology.