Alzheimer disease categorization and fundamental anatomy

Abstract

The pathological features of Alzheimer’s disease include protein buildup, neuronal and synaptic loss, and changes associated with reactive processes. Extracellular antibody buildup manifests in the parenchyma as diffuse, localized, or stellate deposits. It may pertain to the vascular walls of arteries, veins, and capillaries. Instances where the capillary vessel walls are compromised show an elevated likelihood of possessing one or two apoe 4 alleles. Parenchymal and vascular antibody deposition occurs in a sequential manner. Tau accumulation, likely the most significant histological correlate of clinical symptoms, manifests in three forms: inside the neuronal cell body as neurofibrillary tangles, in the dendrites as neuropil threads, and in the axons as the neuritic corona of senile plaques. Tau disease advances in a sequential and predictable manner from the entorhinal cortex, via the hippocampus, to the isocortex. The neuronal loss is variable and particular to certain areas. The mechanism remains a subject of discussion. The timing of synapse loss, likely associated with the Ab peptide, maybe in the form of oligomers, remains contentious. Multiple clinico-pathological variants of Alzheimer disease have been characterized based on lesion type (plaque-only and tangle-predominant), onset type (focal onset), etiology (genetic or spontaneous), and accompanying lesions (Lewy bodies).