The Alzheimer pandemic: is paracetamol to blame?
Identifieur interne : 002020 ( Main/Exploration ); précédent : 002019; suivant : 002021The Alzheimer pandemic: is paracetamol to blame?
Auteurs : Günther Robert Norman Jones [Royaume-Uni]Source :
- Inflammation & allergy drug targets [ 2212-4055 ] ; 2014.
Descripteurs français
- KwdFr :
- Acide peroxynitreux (métabolisme), Acétaminophène (effets indésirables), Acétaminophène (métabolisme), Acétaminophène (usage thérapeutique), Analgésiques non narcotiques (effets indésirables), Analgésiques non narcotiques (usage thérapeutique), Animaux (MeSH), Autoantigènes (immunologie), Autoantigènes (métabolisme), Détoxication de phase I (physiologie), Encéphale (effets des médicaments et des substances chimiques), Histoire du 19ème siècle (MeSH), Histoire du 20ème siècle (MeSH), Histoire du 21ème siècle (MeSH), Humains (MeSH), Maladie d'Alzheimer (histoire), Maladie d'Alzheimer (traitement médicamenteux), Maladie d'Alzheimer (étiologie), Microglie (effets des médicaments et des substances chimiques), Microglie (physiologie), Pandémies (MeSH), Précurseur de la protéine bêta-amyloïde (immunologie), Précurseur de la protéine bêta-amyloïde (métabolisme).
- MESH :
- effets des médicaments et des substances chimiques : Encéphale, Microglie.
- effets indésirables : Acétaminophène, Analgésiques non narcotiques.
- histoire : Maladie d'Alzheimer.
- immunologie : Autoantigènes, Précurseur de la protéine bêta-amyloïde.
- métabolisme : Acide peroxynitreux, Acétaminophène, Autoantigènes, Précurseur de la protéine bêta-amyloïde.
- physiologie : Détoxication de phase I, Microglie.
- traitement médicamenteux : Maladie d'Alzheimer.
- usage thérapeutique : Acétaminophène, Analgésiques non narcotiques.
- étiologie : Maladie d'Alzheimer.
- Animaux, Histoire du 19ème siècle, Histoire du 20ème siècle, Histoire du 21ème siècle, Humains, Pandémies.
English descriptors
- KwdEn :
- Acetaminophen (adverse effects), Acetaminophen (metabolism), Acetaminophen (therapeutic use), Alzheimer Disease (drug therapy), Alzheimer Disease (etiology), Alzheimer Disease (history), Amyloid beta-Protein Precursor (immunology), Amyloid beta-Protein Precursor (metabolism), Analgesics, Non-Narcotic (adverse effects), Analgesics, Non-Narcotic (therapeutic use), Animals (MeSH), Autoantigens (immunology), Autoantigens (metabolism), Brain (drug effects), History, 19th Century (MeSH), History, 20th Century (MeSH), History, 21st Century (MeSH), Humans (MeSH), Metabolic Detoxication, Phase I (physiology), Microglia (drug effects), Microglia (physiology), Pandemics (MeSH), Peroxynitrous Acid (metabolism).
- MESH :
- chemical , adverse effects : Acetaminophen, Analgesics, Non-Narcotic.
- chemical , immunology : Amyloid beta-Protein Precursor, Autoantigens.
- chemical , metabolism : Acetaminophen, Amyloid beta-Protein Precursor, Autoantigens, Peroxynitrous Acid.
- chemical , therapeutic use : Acetaminophen, Analgesics, Non-Narcotic.
- drug effects : Brain, Microglia.
- drug therapy : Alzheimer Disease.
- etiology : Alzheimer Disease.
- history : Alzheimer Disease.
- physiology : Metabolic Detoxication, Phase I, Microglia.
- Animals, History, 19th Century, History, 20th Century, History, 21st Century, Humans, Pandemics.
Abstract
HISTORICAL BACKGROUND
The clinical recognition of a form of dementia closely resembling Alzheimer's disease dates from around 1800. The role of analgesics derived from coal-tar in the spread of the pandemic is traced in terms of the introduction of phenacetin (PN) in 1887; its nephrotoxicity; the observation of lesions characteristic of the disease by Fischer and Alzheimer; the discovery of paracetamol (PA) as the major metabolite of PN; the linking of kidney injury and dementia with high PN usage; and the failure of PN replacement by PA to halt and reverse the exponential, inexorable rise in the incidence of Alzheimer-type dementia. Fischer observed his first case before Alzheimer; it is proposed to rename the syndrome Fischer-Alzheimer disease (F-AD). Disease development: PA-metabolising enzymes are localised in the synaptic areas of the frontal cortex and hippocampus, where F-AD lesions arise. The initiating chemical lesions in liver poisoning comprise covalent binding of a highly reactive product of PA metabolism to proteins; similar events are believed to occur in brain, where alterations in the antigenic profiles of cerebral proteins activate the microglia. β-Amyloid forms, and, like PA itself, induces nitric oxide synthase. Peroxynitrite modifies cerebral proteins by nitrating tyrosine residues, further challenging the microglia and exacerbating the amyloid cascade. Spontaneous reinnervation, N-acetyl cysteine administration and tyrosine supplementation may attenuate the early stages of F-AD development.
CONCLUSION
F-AD is primarily a man-made condition with PA as its principal risk factor.
DOI: 10.2174/1871528112666131219163405
PubMed: 24350947
PubMed Central: PMC3921468
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Acétaminophène</term>
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<term>Précurseur de la protéine bêta-amyloïde</term>
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<front><div type="abstract" xml:lang="en"><p><b>HISTORICAL BACKGROUND</b>
</p>
<p>The clinical recognition of a form of dementia closely resembling Alzheimer's disease dates from around 1800. The role of analgesics derived from coal-tar in the spread of the pandemic is traced in terms of the introduction of phenacetin (PN) in 1887; its nephrotoxicity; the observation of lesions characteristic of the disease by Fischer and Alzheimer; the discovery of paracetamol (PA) as the major metabolite of PN; the linking of kidney injury and dementia with high PN usage; and the failure of PN replacement by PA to halt and reverse the exponential, inexorable rise in the incidence of Alzheimer-type dementia. Fischer observed his first case before Alzheimer; it is proposed to rename the syndrome Fischer-Alzheimer disease (F-AD). Disease development: PA-metabolising enzymes are localised in the synaptic areas of the frontal cortex and hippocampus, where F-AD lesions arise. The initiating chemical lesions in liver poisoning comprise covalent binding of a highly reactive product of PA metabolism to proteins; similar events are believed to occur in brain, where alterations in the antigenic profiles of cerebral proteins activate the microglia. β-Amyloid forms, and, like PA itself, induces nitric oxide synthase. Peroxynitrite modifies cerebral proteins by nitrating tyrosine residues, further challenging the microglia and exacerbating the amyloid cascade. Spontaneous reinnervation, N-acetyl cysteine administration and tyrosine supplementation may attenuate the early stages of F-AD development.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSION</b>
</p>
<p>F-AD is primarily a man-made condition with PA as its principal risk factor.</p>
</div>
</front>
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<Abstract><AbstractText Label="HISTORICAL BACKGROUND" NlmCategory="BACKGROUND">The clinical recognition of a form of dementia closely resembling Alzheimer's disease dates from around 1800. The role of analgesics derived from coal-tar in the spread of the pandemic is traced in terms of the introduction of phenacetin (PN) in 1887; its nephrotoxicity; the observation of lesions characteristic of the disease by Fischer and Alzheimer; the discovery of paracetamol (PA) as the major metabolite of PN; the linking of kidney injury and dementia with high PN usage; and the failure of PN replacement by PA to halt and reverse the exponential, inexorable rise in the incidence of Alzheimer-type dementia. Fischer observed his first case before Alzheimer; it is proposed to rename the syndrome Fischer-Alzheimer disease (F-AD). Disease development: PA-metabolising enzymes are localised in the synaptic areas of the frontal cortex and hippocampus, where F-AD lesions arise. The initiating chemical lesions in liver poisoning comprise covalent binding of a highly reactive product of PA metabolism to proteins; similar events are believed to occur in brain, where alterations in the antigenic profiles of cerebral proteins activate the microglia. β-Amyloid forms, and, like PA itself, induces nitric oxide synthase. Peroxynitrite modifies cerebral proteins by nitrating tyrosine residues, further challenging the microglia and exacerbating the amyloid cascade. Spontaneous reinnervation, N-acetyl cysteine administration and tyrosine supplementation may attenuate the early stages of F-AD development.</AbstractText>
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