Author(s): Anna Kowalska
Journal: Postępy Higieny i Medycyny Doświadczalnej
ISSN 0032-5449
Volume: 63;
Issue: 835515;
Start page: 287;
Date: 2009;
Original page
Keywords: Alzheimer’s Disease | β-amyloid | β-amyloid precursor protein | Dementia | endoproteolysis | fibrillogenesis | neurodegeneration | Neurofibrillary Tangles
ABSTRACT
The brains of AD patients are characterized by cortical atrophy in the form of gyral shrinkage, widening of the sulci, and enlargement of the ventricles. The first regions to be affected are the hippocampus and entorhinal cortex. At later stages of the disease appear: 1) accumulation of extracellular senile plaques (disturbed App protein metabolism), 2) intracellular aggregation of neurofibrillary tangles (the tau protein pathology), 3) synaptic degeneration, and 4) the death (usually due to apoptosis, rarely due to necrosis) of selected populations of neuronal cells as the neuropathological hallmarks of AD throughout the whole brain. The solution to the mystery of AD’s pathogenesis is based on our understanding of the mechanisms of β-amyloid (Aβ) generation and oligomerization as well as the molecular basis of its neurotoxicity, but primarily on an accurate account of the role of Aβ in cell metabolism.
Journal: Postępy Higieny i Medycyny Doświadczalnej
ISSN 0032-5449
Volume: 63;
Issue: 835515;
Start page: 287;
Date: 2009;
Original page
Keywords: Alzheimer’s Disease | β-amyloid | β-amyloid precursor protein | Dementia | endoproteolysis | fibrillogenesis | neurodegeneration | Neurofibrillary Tangles
ABSTRACT
The brains of AD patients are characterized by cortical atrophy in the form of gyral shrinkage, widening of the sulci, and enlargement of the ventricles. The first regions to be affected are the hippocampus and entorhinal cortex. At later stages of the disease appear: 1) accumulation of extracellular senile plaques (disturbed App protein metabolism), 2) intracellular aggregation of neurofibrillary tangles (the tau protein pathology), 3) synaptic degeneration, and 4) the death (usually due to apoptosis, rarely due to necrosis) of selected populations of neuronal cells as the neuropathological hallmarks of AD throughout the whole brain. The solution to the mystery of AD’s pathogenesis is based on our understanding of the mechanisms of β-amyloid (Aβ) generation and oligomerization as well as the molecular basis of its neurotoxicity, but primarily on an accurate account of the role of Aβ in cell metabolism.
