0000000000395181
AUTHOR
Jose Carlos Davila
Dual roles of Aβ in proliferative processes in an amyloidogenic model of Alzheimer’s disease
Alzheimer’s disease is a major neurodegenerative disorder that leads to severe cognitive deficits in the elderly population. Over the past two decades, multiple studies have focused on elucidating the causative factors underlying memory defects in Alzheimer’s patients. In this regard, new evidence linking Alzheimer’s disease-related pathology and neuronal stem cells suggests that hippocampal neurogenesis impairment is an important factor underlying these cognitive deficits. However, because of conflicting results, the impact of Aβ pathology on neurogenesis/gliogenesis remains unclear. Here, we investigated the effect of Aβ on neuronal and glial proliferation by using an APP/PS1 transgenic m…
Calcium-binding proteins in the dorsal ventricular ridge of the lizardPsammodromus algirus
The aim of the present work was to study further the intrinsic organization of the dorsal ventricular ridge of lizards. For that purpose, the morphology and distribution of cells and fibers containing the calcium-binding proteins calbindin-D28k, parvalbumin, and calretinin were investigated by using immunohistochemical methods. Colocalization of calcium-binding proteins with the neurotransmitter gamma-aminobutyric acid (GABA) was also studied because they are shown to coexist in many areas of the telencephalon where they define distinct subpopulations of GABAergic local circuit neurons. Neurons containing calcium-binding proteins are limited to the anterior part of the dorsal ventricular ri…
Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer's mice hippocampus
Dystrophic neurites associated with amyloid plaques precede neuronal death and manifest early in Alzheimer's disease (AD). In this work we have characterized the plaque-associated neuritic pathology in the hippocampus of young (4- to 6-month-old) PS1(M146L)/APP(751SL) mice model, as the initial degenerative process underlying functional disturbance prior to neuronal loss. Neuritic plaques accounted for almost all fibrillar deposits and an axonal origin of the dystrophies was demonstrated. The early induction of autophagy pathology was evidenced by increased protein levels of the autophagosome marker LC3 that was localized in the axonal dystrophies, and by electron microscopic identification…