Immunoelectron microscopic study of synaptic pathology in Alzheimer's disease

1991 ◽  
Vol 81 (4) ◽  
pp. 428-433 ◽  
Author(s):  
E. Masliah ◽  
L. Hansen ◽  
T. Albright ◽  
M. Mallory ◽  
R. D. Terry
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Microscopic Study ◽  
Synaptic Pathology

P2-101: EVALUATION OF THE PRESYNAPTIC PROTEIN SNAP-25 AS A NOVEL CEREBROSPINAL FLUID MARKER FOR SYNAPTIC PATHOLOGY IN ALZHEIMER'S DISEASE

2014 ◽  
Vol 10 ◽  
pp. P508-P508
Author(s):  
Annika Öhrfelt ◽  
Gunnar Brinkmalm ◽  
William G. Honer ◽  
Lutz Frölich ◽  
Lucrezia Hausner ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Synaptic Pathology ◽  
Presynaptic Protein

scholarly journals Dysfunction of the ubiquitin ligase E3A Ube3A/E6-AP contributes to synaptic pathology in Alzheimer’s disease

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Markel Olabarria ◽  
Silvia Pasini ◽  
Carlo Corona ◽  
Pablo Robador ◽  
Cheng Song ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Ubiquitin Ligase ◽  
Synaptic Pathology

scholarly journals Mitochondria Are Related to Synaptic Pathology in Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Stavros J. Baloyannis
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dendritic Spines ◽  
Red Nucleus ◽  
Morphological Alterations ◽  
Mitochondrial Alterations ◽  
Amyloid Deposits ◽  
Synaptic Pathology ◽  
Autopsy Specimens ◽  
Dendritic Branches

Morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer's disease, been associated with oxidative stress and Aβ-peptide-induced toxicity. We proceeded to estimation of mitochondria on electron micrographs of autopsy specimens of Alzheimer's disease. We found substantial morphological and morphometric changes of the mitochondria in the neurons of the hippocampus, the neocortex, the cerebellar cortex, the thalamus, the globus pallidus, the red nucleus, the locus coeruleus, and the climbing fibers. The alterations consisted of considerable changes of the cristae, accumulation of osmiophilic material, and modification of the shape and size. Mitochondrial alterations were prominent in neurons, which showed a depletion of dendritic spines and loss of dendritic branches. Mitochondrial alterations are not related with the accumulation of amyloid deposits, but are prominent whenever fragmentation of the Golgi apparatus exists. Morphometric analysis showed also that mitochondria are significantly reduced in neurons, which demonstrated synaptic pathology.

Neurochemical Dissection of Synaptic Pathology in Alzheimer's Disease

1998 ◽  
Vol 10 (1) ◽  
pp. 11-23 ◽  
Author(s):  
Pia Davidsson ◽  
Kaj Blennow
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Cortex ◽  
Late Onset ◽  
Synaptic Proteins ◽  
Presynaptic Membrane ◽  
Control Value ◽  
Postsynaptic Protein ◽  
Post Mortem Brain ◽  
Synaptic Pathology

Synaptic pathology has attained increasing attention as being central in the pathogenesis of Alzheimer's disease (AD). To address the question whether synaptic pathology in AD involves the whole synapse, or is limited to specific components thereof, we studied three different synaptic vesicle proteins (rab3a, synaptotagmin, synaptophysin) and also the presynaptic membrane protein GAP-43 and the postsynaptic protein neurogranin. The material included post-mortem brain tissue (frontal cortex, hippocampus, and cerebellum) from 8 patients with early-onset AD (EAD), 11 patients with late-onset AD (LAD), 6 patients with vascular dementia (VAD), and 9 control subjects. A reduction of all synaptic proteins was found in AD, more pronounced in EAD than in LAD, in both the frontal cortex (EAD 30% to 70% vs. LAD 82% to 88% of control value) and hippocampus (EAD 22% to 82% vs. LAD 76% to 89% of control value), whereas only minor changes were found in VAD. The finding that all synaptic proteins were reduced in AD suggests a degeneration and loss of whole synaptic elements that are more pronounced in EAD than in LAD.

Thrombospondin-1 prevents amyloid beta–mediated synaptic pathology in Alzheimer's disease

2015 ◽  
Vol 36 (12) ◽  
pp. 3214-3227 ◽  
Author(s):  
Sung Min Son ◽  
Dong Woo Nam ◽  
Moon-Yong Cha ◽  
Kyung Ho Kim ◽  
Jayoung Byun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Thrombospondin 1 ◽  
Synaptic Pathology
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