Deciphering the molecular basis of memory failure in Alzheimer's disease.

TL;DR: Past observations are synthesized to provide strong evidence that the default network is a specific, anatomically defined brain system preferentially active when individuals are not focused on the external environment, and for understanding mental disorders including autism, schizophrenia, and Alzheimer's disease.

TL;DR: To identify regions of high connectivity in the human cerebral cortex, a computationally efficient approach was applied to map the degree of intrinsic functional connectivity across the brain and explored whether the topography of hubs could explain the pattern of vulnerability in Alzheimer's disease (AD).

TL;DR: It is reported that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus.

TL;DR: Reliance on reserve is emerging as an important factor that determines who ages gracefully and who declines rapidly, and increased recruitment of brain areas in older adults may reflect a form of compensation.

TL;DR: In this article, photo-induced cross-linking of unmodified proteins (PICUP) was combined with size-exclusion chromatography, dynamic light scattering, circular dichroism spectroscopy, and electron microscopy to reveal the early assembly of Aβ40 and Aβ42.

TL;DR: It is shown that overexpression of FAD(717V-->F)-mutant human APP in neurons of transgenic mice decreases the density of presynaptic terminals and neurons well before these mice develop amyloid plaques, suggesting a neurotoxic effect of Abeta that is independent of plaque formation.

TL;DR: Protofibrils appeared during the polymerization of Abeta-(1-40), Abeta-1-42, and Abeta)-Gln22, peptides associated with both sporadic and inherited forms of Alzheimer's disease, suggesting that protofibril formation may be a general phenomenon in Abeta fibrillogenesis.

TL;DR: Colocalization of ApoE and LRP to SPs implies that these molecules may be involved in metabolism of components of SPs, and it is suggested that SPs and reactive astrocytes were also strongly LRP immunoreactive in Alzheimer's disease.