Biological Pathway Taxonomy

Last uploaded: March 30, 2022
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Id urn:agi-pathway:uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
urn:agi-pathway:uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
Preferred Name

Alzheimer's Disease
Synonyms
Organ_System: nervous system
PathwayType: signaling
Description: The most important events in pathogenesis of Alzheimer's disease (AD) are neurofibrillary tangles (NFTs) and amyloid plaques formation. Pathway is built manually using published studies.
Organ: brain
Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101
PMID: 15910549
PMID: 16768248
Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
PMID: 22257884
NodeType: Pathway
Notes: Headnote: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with symptoms including short-term memory loss, disorientation, problems with self care, mood swings, and behavioural issues. AD is characterized by the formation of amyloid plaques (deposits of amyloid beta peptide (Abeta) outside the cells) and neurofibrillary tangles (aggregates of hyperphosphorylated microtubule-associated protein tau (MAPT) inside the neurons). About 5% of AD cases are the early-onset familial form, where a genetic predisposition leads to the disease. The genes involved are APP, PSEN1, and PSEN2. Signaling description: Abeta is derived from the amyloid precursor protein (APP) via sequential proteolysis by beta-secretase (BACE1) and gamma-secretase. MME, ACE, IDE, and ECE1 normally cleave Abeta, but become decreased in AD. The neurofibrillary tangles are formed when MAPT becomes hyper-phosphorylated with GSK3B being one of the major enzymes participating in this process. These processes are triggered and progressed by calcium (Ca2+) overload, which is provoked by the excessive ion influx into the neuron through specific ion channels, such as the voltage-gated calcium channels (VGCCs) and several ligand-gated ion channels (N-methyl-D-aspartate selective glutamate receptor or NMDAR, CHRM1, and CHRNA7). The channels open when Abeta binds to them. Abeta also interacts with TNFRSF1A promoting caspase cascade activation. Outcome effects: Caspase cascade activation directs the cells to apoptosis. Ca2+ also induces mitochondrial dysfunction by activating proapoptotic factors such as CYCS, ENDOG, and AIFM1. Finally,NFTs cause a disruption in intracellular transport and dendrite degradation triggering cell death. Highlighted proteins: Entities with increased expression or activity are highlighted in red, and entities with decreased expression or activity are highlighted in blue. Mutated genes: Mutated genes are shown in white-out style.
CellType: neuron
Source: Diseases
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Type http://www.w3.org/2002/07/owl#Class

All Properties

label
Alzheimer's Disease
prefLabel
Alzheimer's Disease
database_cross_reference
PS:PathwayType
PS:Description
PS:Pathway_Author
PS:Link
PS:CellType
PS:Organ_System
PS:PMID
PS:NodeType
PS:Notes
PS:Organ
PS:Source
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notation
uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
id
urn:agi-pathway:uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
subClassOf
urn:agi-folder:a
urn:agi-folder:nervous_system
urn:agi-folder:aging_related_diseases
urn:agi-folder:alzheimer's_disease
type
has_exact_synonym
Organ_System: nervous system
PathwayType: signaling
Description: The most important events in pathogenesis of Alzheimer's disease (AD) are neurofibrillary tangles (NFTs) and amyloid plaques formation. Pathway is built manually using published studies.
Organ: brain
Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101
PMID: 15910549
PMID: 16768248
Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-a249b5e2-83c9-4caa-a9df-bb050fcdaeb7
PMID: 22257884
NodeType: Pathway
Notes: Headnote: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with symptoms including short-term memory loss, disorientation, problems with self care, mood swings, and behavioural issues. AD is characterized by the formation of amyloid plaques (deposits of amyloid beta peptide (Abeta) outside the cells) and neurofibrillary tangles (aggregates of hyperphosphorylated microtubule-associated protein tau (MAPT) inside the neurons). About 5% of AD cases are the early-onset familial form, where a genetic predisposition leads to the disease. The genes involved are APP, PSEN1, and PSEN2. Signaling description: Abeta is derived from the amyloid precursor protein (APP) via sequential proteolysis by beta-secretase (BACE1) and gamma-secretase. MME, ACE, IDE, and ECE1 normally cleave Abeta, but become decreased in AD. The neurofibrillary tangles are formed when MAPT becomes hyper-phosphorylated with GSK3B being one of the major enzymes participating in this process. These processes are triggered and progressed by calcium (Ca2+) overload, which is provoked by the excessive ion influx into the neuron through specific ion channels, such as the voltage-gated calcium channels (VGCCs) and several ligand-gated ion channels (N-methyl-D-aspartate selective glutamate receptor or NMDAR, CHRM1, and CHRNA7). The channels open when Abeta binds to them. Abeta also interacts with TNFRSF1A promoting caspase cascade activation. Outcome effects: Caspase cascade activation directs the cells to apoptosis. Ca2+ also induces mitochondrial dysfunction by activating proapoptotic factors such as CYCS, ENDOG, and AIFM1. Finally,NFTs cause a disruption in intracellular transport and dendrite degradation triggering cell death. Highlighted proteins: Entities with increased expression or activity are highlighted in red, and entities with decreased expression or activity are highlighted in blue. Mutated genes: Mutated genes are shown in white-out style.
CellType: neuron
Source: Diseases
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urn:agi-folder:a
urn:agi-folder:nervous_system
urn:agi-folder:aging_related_diseases
urn:agi-folder:alzheimer's_disease
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