Protective potential of glucagon like peptide 2 (GLP-2) against the neurodegeneration

Risultato della ricerca: Article

Abstract

Neurodegeneration consists in loss of neuron specific types, pattern and distribution, leading to progressive dysfunctions of the central nervous system. Neurodegenerative diseases include diverse pathological conditions, among which Alzheimer’s and Parkinson’s diseases are the most prevalent ones. Alzheimer’s disease is known as a growing dementia, characterized by progressive language, memory, and cognitive loss, while Parkinson’s disease is primarily characterized as a motor disorder. Senile plaques, caused by amyloid β peptide, hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of Alzheimer’s disease. Amyloid β oligomer formation is associated with development of reactive oxygen and nitrogen species, inflammation, calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions related with learning and memory. Parkinson’s disease is produced by dopaminergic neuron deterioration in the extrapyramidal tract of the midbrain. Accumulation of α-synuclein proteins (Lewy bodies) in the central, autonomic, and peripheral nervous system is the hallmark of the Parkinson’s disease. The Levy bodies break the neuronal membrane leading to neuronal death through oxidative stress, excitotoxicity, energy failure and neuroinflammation.
Lingua originaleEnglish
pagine (da-a)1901-1902
Numero di pagine2
RivistaNeural Regeneration Research
Volume14
Stato di pubblicazionePublished - 2019

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Glucagon-Like Peptide 2
Parkinson Disease
Alzheimer Disease
Amyloid
Extrapyramidal Tracts
Central Nervous System
Synucleins
Cell Respiration
Lewy Bodies
Reactive Nitrogen Species
Neurofibrillary Tangles
Dopaminergic Neurons
Autonomic Nervous System
Amyloid Plaques
Memory Disorders
Peripheral Nervous System
Mesencephalon
Neurodegenerative Diseases
Synapses
Dementia

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience

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title = "Protective potential of glucagon like peptide 2 (GLP-2) against the neurodegeneration",
abstract = "Neurodegeneration consists in loss of neuron specific types, pattern and distribution, leading to progressive dysfunctions of the central nervous system. Neurodegenerative diseases include diverse pathological conditions, among which Alzheimer’s and Parkinson’s diseases are the most prevalent ones. Alzheimer’s disease is known as a growing dementia, characterized by progressive language, memory, and cognitive loss, while Parkinson’s disease is primarily characterized as a motor disorder. Senile plaques, caused by amyloid β peptide, hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of Alzheimer’s disease. Amyloid β oligomer formation is associated with development of reactive oxygen and nitrogen species, inflammation, calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions related with learning and memory. Parkinson’s disease is produced by dopaminergic neuron deterioration in the extrapyramidal tract of the midbrain. Accumulation of α-synuclein proteins (Lewy bodies) in the central, autonomic, and peripheral nervous system is the hallmark of the Parkinson’s disease. The Levy bodies break the neuronal membrane leading to neuronal death through oxidative stress, excitotoxicity, energy failure and neuroinflammation.",
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AB - Neurodegeneration consists in loss of neuron specific types, pattern and distribution, leading to progressive dysfunctions of the central nervous system. Neurodegenerative diseases include diverse pathological conditions, among which Alzheimer’s and Parkinson’s diseases are the most prevalent ones. Alzheimer’s disease is known as a growing dementia, characterized by progressive language, memory, and cognitive loss, while Parkinson’s disease is primarily characterized as a motor disorder. Senile plaques, caused by amyloid β peptide, hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of Alzheimer’s disease. Amyloid β oligomer formation is associated with development of reactive oxygen and nitrogen species, inflammation, calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions related with learning and memory. Parkinson’s disease is produced by dopaminergic neuron deterioration in the extrapyramidal tract of the midbrain. Accumulation of α-synuclein proteins (Lewy bodies) in the central, autonomic, and peripheral nervous system is the hallmark of the Parkinson’s disease. The Levy bodies break the neuronal membrane leading to neuronal death through oxidative stress, excitotoxicity, energy failure and neuroinflammation.

UR - http://hdl.handle.net/10447/362108

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