Alzheimer’s Disease

Abstract

The gradual development of Alzheimer-related neurofibrillary changes and β-amyloid deposits have been investigated in the amygdala and cerebral cortex with advanced silver methods. Neurofibrillary tangles occur within the somata of nerve cells, while neuropil threads are located in nerve cell processes. In neuritic plaques, there are both neuronal processes containing neurofibrillary changes and extracellular deposits of β-amyloid protein. The amygdala early displays Alzheimer-type pathology and is typically rich in neuritic plaques. Neuritic plaques do not occur in the amygdala in the absence of neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala. In contrast to the gradual increase in the number of neurofibrillary tangles and neuropil threads, neuritic plaques grow in size and number along with advancement in the neurofibrillary and β-amyloid pathology. The findings indicate that neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala precede neuritic plaques in the amygdala, and the density of neuritic plaques is related both to the degree of neurofibrillary and β-amyloid pathology in the cerebral cortex.

High-resolution magnetic resonance imaging reveals nuclei of the human amygdala: manual segmentation to automatic atlas

“…For the ADNI comparison, we expected gross anatomical differences between the pathological and the control group, given the neuropathology in AD and MCI (Merkesbery, 2010; Yilmazer-Hanke, 1998). In contrast, we expected rather small (if any) differences for the ABIDE group comparison.…”

“…Adolphs et al, 2005, Kliemann et al 2012, Hortensius et al, 2016), and accordingly, its dysfunction is implicated in psychopathologies, such as mood disorders (Phillips et al, 2003; Siegle et al, 2002), anxiety disorders (Birbaumer et al, 1998; Rauch et al, 2003), and developmental disorders (Baron-Cohen et al, 2000; Dziobek et al, 2010). Additionally, several post mortem studies have shown that the amygdala is a common site for neurofibrillary tangles and senile plaques in mild cognitive impairment (Merkesbery, 2010) and Alzheimer’s disease (Yilmazer-Hanke, 1998) as well as Lewy bodies (Kotzbauer et al, 2011, Fujishiro et al, 2002). …”

Processing of cdk5 Activator p35 to Its Truncated Form (p25) by Calpain in Acutely Injured Neuronal Cells

“…A phospho-Tau antibody AT8 was used, which detects Tau phosphorylated dually at S202 and T205. This antibody has been shown to only detect abnormally hyperphosphorylated Tau in Alzheimer's brains (28,29). Indeed, there was almost no AT8 P-tau signal in naïve or vehicle-injected rat brains (Fig.…”