More than 100 years after description of Alzheimer's disease (AD), two major pathological
processes observed already by Alois Alzheimer, remain as the main explanation of the …

Cytoskeletal abnormalities and synaptic loss, typical of both familial and sporadic Alzheimer
disease (AD), are induced by diverse stresses such as neuroinflammation, oxidative stress …

Abstract Background Loss of the Sortilin-related receptor 1 (SORL1) gene seems to act as a
causal event for Alzheimer's disease (AD). Recent studies have established that loss of …

Lipid rafts are membrane domains, more ordered than the bulk membrane and enriched in
cholesterol and sphingolipids. They represent a platform for protein-lipid and protein–protein …

Zinc dyshomeostasis has been recognized as an important mechanism for cell death in
acute brain injury. An increase in the level of free or histochemically reactive zinc in …

In Alzheimer's disease (AD), numerous β-amyloid (Aβ) plaques are associated with
butyrylcholinesterase (BChE) activity, the significance of which is unclear. A mouse model …

In Alzheimer's disease (AD), the canonical Wnt inhibitor Dickkopf-1 (Dkk1) is induced by β-
amyloid (Aβ) and shifts the balance from canonical towards non-canonical Wnt signalling …

Axonal generation of Alzheimer's disease (AD)-associated amyloid-β (Aβ) plays a key role in
AD neuropathology, but the cellular mechanisms involved in its release have remained …

Alzheimer's disease (AD) is characterized by toxic protein accumulation in the brain.
Ubiquitination is essential for protein clearance in cells, making altered ubiquitin signaling …

Carboxypeptidase E (CPE) or carboxypeptidase H was first discovered in 1982 as an
enkephalin-convertase that cleaved a C-terminal basic residue from enkephalin precursors …