Columnar arragement of ?-amyloid protein deposits in the cerebral cortex of patients with Alzheimer's disease

1993 ◽  
Vol 85 (4) ◽  
pp. 400-403 ◽  
Author(s):  
H. Akiyama ◽  
T. Yamada ◽  
P. L. McGeer ◽  
T. Kawamata ◽  
I. Tooyama ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Amyloid Protein ◽  
Protein Deposits

scholarly journals Phosphoinositides signaling modulates microglial actin remodeling and phagocytosis in Alzheimer’s disease

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Smita Eknath Desale ◽  
Subashchandrabose Chinnathambi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Amyloid Β ◽  
Dietary Fatty Acids ◽  
Receptor Expression ◽  
Actin Binding ◽  
Actin Remodeling ◽  
Protein Deposits

AbstractAlzheimer’s disease is one of the neurodegenerative diseases, characterized by the accumulation of abnormal protein deposits, which disrupts signal transduction in neurons and other glia cells. The pathological protein in neurodegenerative diseases, Tau and amyloid-β contribute to the disrupted microglial signaling pathways, actin cytoskeleton, and cellular receptor expression. The important secondary messenger lipids i.e., phosphatidylinositols are largely affected by protein deposits of amyloid-β in Alzheimer’s disease. Phosphatidylinositols are the product of different phosphatidylinositol kinases and the state of phosphorylation at D3, D4, and D5 positions of inositol ring. Phosphatidylinositol 3,4,5-triphosphate (PI 3, 4, 5-P3) involves in phagocytic cup formation, cell polarization, whereas Phosphatidylinositol 4,5-bisphosphate (PI 4, 5-P2)-mediates the process of phagosomes formation and further its fusion with early endosome.. The necessary activation of actin-binding proteins such as Rac, WAVE complex, and ARP2/3 complex for the actin polymerization in the process of phagocytosis, migration is regulated and maintained by PI 3, 4, 5-P3 and PI 4, 5-P2. The ratio and types of fatty acid intake can influence the intracellular secondary lipid messengers along with the cellular content of phaphatidylcholine and phosphatidylethanolamine. The Amyloid-β deposits and extracellular Tau seeds disrupt phosphatidylinositides level and actin cytoskeletal network that hamper microglial-signaling pathways in AD. We hypothesize that being a lipid species intracellular levels of phosphatidylinositol would be regulated by dietary fatty acids. Further we are interested to understand phosphoinositide-based signaling cascades in phagocytosis and actin remodeling.

Alzheimer's disease-type neurofibrillary degeneration in verrucose dysplasias of the cerebral cortex

1995 ◽  
Vol 90 (4) ◽  
pp. 356-365 ◽  
Author(s):  
M. A. Mor�n ◽  
A. Probst ◽  
C. Navarro ◽  
P. G�mez-Ramos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Disease Type ◽  
Neurofibrillary Degeneration

Intralaminar Distribution of Neurotransmitter-Related Enzymes in Cerebral Cortex of Alzheimer’s Disease

Gerontology ◽  
1987 ◽  
Vol 33 (3-4) ◽  
pp. 197-202 ◽  
Author(s):  
Sandro Sorbi ◽  
Silvia Piacentini ◽  
Luigi Amaducci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex
Sign in / Sign up

Export Citation Format

Share Document