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Article ; Online: Iron Responsiveness to Lysosomal Disruption: A Novel Pathway to Alzheimer's Disease.

Rogers, Jack T / Cahill, Catherine M

2023 Volume 96, Issue 1, Page(s) 41–45

Abstract: Familial Alzheimer's disease (fAD) mutations in the amyloid-β protein precursor (AβPP) enhance brain AβPP C-Terminal Fragment (CTF) levels to inhibit lysosomal v-ATPase. Consequent disrupted acidification of the endolysosomal pathway may trigger brain ... ...

Abstract	Familial Alzheimer's disease (fAD) mutations in the amyloid-β protein precursor (AβPP) enhance brain AβPP C-Terminal Fragment (CTF) levels to inhibit lysosomal v-ATPase. Consequent disrupted acidification of the endolysosomal pathway may trigger brain iron deficiencies and mitochondrial dysfunction. The iron responsive element (IRE) in the 5'Untranslated-region of AβPP mRNA should be factored into this cycle where reduced bioavailable Fe-II would decrease IRE-dependent AβPP translation and levels of APP-CTFβ in a cycle to adaptively restore iron homeostasis while increases of transferrin-receptors is evident. In healthy younger individuals, Fe-dependent translational modulation of AβPP is part of the neuroprotective function of sAβPPα with its role in iron transport.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Iron/metabolism ; Protein Biosynthesis ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Lysosomes/metabolism ; Amyloid beta-Peptides/metabolism
Chemical Substances	Iron (E1UOL152H7) ; Amyloid beta-Protein Precursor ; Amyloid beta-Peptides
Language	English
Publishing date	2023-10-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230953
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Zs.A 6084: Show issues

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Article ; Online: Opioid dose regimen shapes mesolimbic adaptations.

Cahill, Catherine M

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2020 Volume 45, Issue 11, Page(s) 1777–1778

MeSH term(s)	Analgesics, Opioid ; Narcotic Antagonists ; Receptors, Opioid, mu
Chemical Substances	Analgesics, Opioid ; Narcotic Antagonists ; Receptors, Opioid, mu
Keywords	covid19
Language	English
Publishing date	2020-04-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-020-0679-y
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Zs.A 2379: Show issues

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Article ; Online: Unveiling the link between chronic pain and misuse of opioids and cannabis.

Dagher, Merel / Alayoubi, Myra / Sigal, Gabriella H / Cahill, Catherine M

Journal of neural transmission (Vienna, Austria : 1996)

2024 Volume 131, Issue 5, Page(s) 563–580

Abstract: Over 50 million Americans endure chronic pain where many do not receive adequate treatment and self-medicate to manage their pain by taking substances like opioids and cannabis. Research has shown high comorbidity between chronic pain and substance use ... ...

Abstract	Over 50 million Americans endure chronic pain where many do not receive adequate treatment and self-medicate to manage their pain by taking substances like opioids and cannabis. Research has shown high comorbidity between chronic pain and substance use disorders (SUD) and these disorders share many common neurobiological underpinnings, including hypodopaminergic transmission. Drugs commonly used for self-medication such as opioids and cannabis relieve emotional, bothersome components of pain as well as negative emotional affect that perpetuates misuse and increases the risk of progressing towards drug abuse. However, the causal effect between chronic pain and the development of SUDs has not been clearly established. In this review, we discuss evidence that affirms the proposition that chronic pain is a risk factor for the development of opioid and cannabis use disorders by outlining the clinical evidence and detailing neurobiological mechanisms that link pain and drug misuse. Central to the link between chronic pain and opioid and cannabis misuse is hypodopaminergic transmission and the modulation of dopamine signaling in the mesolimbic pathway by opioids and cannabis. Moreover, we discuss the role of kappa opioid receptor activation and neuroinflammation in the context of dopamine transmission, their contribution to opioid and cannabis withdrawal, along with potential new treatments.
MeSH term(s)	Humans ; Chronic Pain/drug therapy ; Chronic Pain/physiopathology ; Analgesics, Opioid/adverse effects ; Opioid-Related Disorders ; Animals ; Marijuana Abuse/complications ; Marijuana Abuse/physiopathology
Chemical Substances	Analgesics, Opioid
Language	English
Publishing date	2024-04-03
Publishing country	Austria
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	184163-4
ISSN	1435-1463 ; 0300-9564
ISSN (online)	1435-1463
ISSN	0300-9564
DOI	10.1007/s00702-024-02765-3
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Ui II Zs.150: Show issues

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Article: Editorial: Broadening our conceptual understanding of endogenous opioids in systems neuroscience.

Tejeda, Hugo A / Massaly, Nicolas / Corder, Gregory / Cahill, Catherine M

Frontiers in systems neuroscience

2023 Volume 17, Page(s) 1212650

Language	English
Publishing date	2023-06-13
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2453005-0
ISSN	1662-5137
ISSN	1662-5137
DOI	10.3389/fnsys.2023.1212650
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Article ; Online: Opioid Systems and Depression: The Relationship Is Strengthening.

Dagher, Merel / Cahill, Catherine M / Evans, Christopher J

Biological psychiatry

2022 Volume 92, Issue 12, Page(s) 920–922

MeSH term(s)	Humans ; Analgesics, Opioid/adverse effects ; Depression ; Opioid-Related Disorders
Chemical Substances	Analgesics, Opioid
Language	English
Publishing date	2022-11-14
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2022.09.020
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Zs.A 720: Show issues

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Article ; Online: Iron-responsive-like elements and neurodegenerative ferroptosis.

Rogers, Jack T / Cahill, Catherine M

Learning & memory (Cold Spring Harbor, N.Y.)

2020 Volume 27, Issue 9, Page(s) 395–413

Abstract: A set of common-acting iron-responsive 5'untranslated region (5'UTR) motifs can fold into RNA stem loops that appear significant to the biology of cognitive declines of Parkinson's disease dementia (PDD), Lewy body dementia (LDD), and Alzheimer's disease ...

Abstract	A set of common-acting iron-responsive 5'untranslated region (5'UTR) motifs can fold into RNA stem loops that appear significant to the biology of cognitive declines of Parkinson's disease dementia (PDD), Lewy body dementia (LDD), and Alzheimer's disease (AD). Neurodegenerative diseases exhibit perturbations of iron homeostasis in defined brain subregions over characteristic time intervals of progression. While misfolding of Aβ from the amyloid-precursor-protein (APP), alpha-synuclein, prion protein (PrP) each cause neuropathic protein inclusions in the brain subregions, iron-responsive-like element (IRE-like) RNA stem-loops reside in their transcripts. APP and αsyn have a role in iron transport while gene duplications elevate the expression of their products to cause rare familial cases of AD and PDD. Of note, IRE-like sequences are responsive to excesses of brain iron in a potential feedback loop to accelerate neuronal ferroptosis and cognitive declines as well as amyloidosis. This pathogenic feedback is consistent with the translational control of the iron storage protein ferritin. We discuss how the IRE-like RNA motifs in the 5'UTRs of APP, alpha-synuclein and PrP mRNAs represent uniquely folded drug targets for therapies to prevent perturbed iron homeostasis that accelerates AD, PD, PD dementia (PDD) and Lewy body dementia, thus preventing cognitive deficits. Inhibition of alpha-synuclein translation is an option to block manganese toxicity associated with early childhood cognitive problems and manganism while Pb toxicity is epigenetically associated with attention deficit and later-stage AD. Pathologies of heavy metal toxicity centered on an embargo of iron export may be treated with activators of APP and ferritin and inhibitors of alpha-synuclein translation.
MeSH term(s)	5' Untranslated Regions/drug effects ; Amyloid beta-Peptides/drug effects ; Amyloid beta-Peptides/metabolism ; Animals ; Ferritins/drug effects ; Ferritins/metabolism ; Ferroptosis/drug effects ; Ferroptosis/physiology ; Heavy Metal Poisoning/drug therapy ; Heavy Metal Poisoning/metabolism ; Heavy Metal Poisoning/physiopathology ; Humans ; Iron-Regulatory Proteins/drug effects ; Iron-Regulatory Proteins/metabolism ; Neurocognitive Disorders/drug therapy ; Neurocognitive Disorders/metabolism ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/metabolism ; Neuroprotective Agents/pharmacology ; Protein Biosynthesis/drug effects ; alpha-Synuclein/drug effects ; alpha-Synuclein/metabolism
Chemical Substances	5' Untranslated Regions ; Amyloid beta-Peptides ; Iron-Regulatory Proteins ; Neuroprotective Agents ; alpha-Synuclein ; Ferritins (9007-73-2)
Language	English
Publishing date	2020-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1204777-6
ISSN	1549-5485 ; 1072-0502
ISSN (online)	1549-5485
ISSN	1072-0502
DOI	10.1101/lm.052282.120
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Zs.A 4107: Show issues

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Article: Evidence and Function Relevance of Native DOR-MOR Heteromers.

Cahill, Catherine M / Ong, Edmund

Handbook of experimental pharmacology

2018 Volume 247, Page(s) 115–127

Abstract: ... heteromers. Owing to their constituent monomers' involvement in analgesia, mu/delta opioid receptor (M/DOR ... indisputable proof of M/DOR formation in vivo are still evolving. This aspect of the field has been slow ...

Abstract	Opioid receptors are the sites of action for morphine and most other clinically used opioid drugs. Abundant evidence now demonstrates that different opioid receptor types can physically associate to form heteromers. Owing to their constituent monomers' involvement in analgesia, mu/delta opioid receptor (M/DOR) heteromers have been a particular focus of attention. Understandings of the physiological relevance and indisputable proof of M/DOR formation in vivo are still evolving. This aspect of the field has been slow to progress in large part by the limitations of most available experimental models; recently however, promising progress is being made. As a result, the long-repeated promise of opioid receptor heteromers as selective therapeutic targets is now being realized.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Drug Design ; Humans ; Ligands ; Protein Multimerization ; Receptors, Opioid, delta/drug effects ; Receptors, Opioid, delta/physiology ; Receptors, Opioid, mu/drug effects ; Receptors, Opioid, mu/physiology
Chemical Substances	Analgesics, Opioid ; Ligands ; OPRM1 protein, human ; Receptors, Opioid, delta ; Receptors, Opioid, mu
Language	English
Publishing date	2018-03-26
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/164_2018_112
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Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
danach: Sign. bei den Einzelbänden: Show issues

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Article ; Online: Fentanyl: Receptor pharmacology, abuse potential, and implications for treatment.

Comer, Sandra D / Cahill, Catherine M

Neuroscience and biobehavioral reviews

2018 Volume 106, Page(s) 49–57

Abstract: Opioid overdoses, many of which are attributed to use of illicit fentanyl, are currently one of the leading causes of death in the U.S. Although fentanyl has been used safely for decades in clinical settings, the widespread use of illicit fentanyl is a ... ...

Abstract	Opioid overdoses, many of which are attributed to use of illicit fentanyl, are currently one of the leading causes of death in the U.S. Although fentanyl has been used safely for decades in clinical settings, the widespread use of illicit fentanyl is a recent phenomenon. Starting in 2013, illicitly manufactured fentanyl and its analogs began to appear on the streets. These substances were added to or sold as heroin, often unbeknownst to the user. Because fentanyl is so potent, only small amounts are needed to produce pharmacological effects, but the margin between safe and toxic doses is narrow. Surprisingly little is known about the exact signaling mechanisms underlying fentanyl-related respiratory depression or the effectiveness of naloxone in reversing this effect. Similarly, little is known about the ability of treatment medications such as buprenorphine, methadone, or naltrexone to reduce illicit fentanyl use. The present article reviews the receptor, preclinical and clinical pharmacology of fentanyl, and how its pharmacology may predict the effectiveness of currently approved medications for treating illicit fentanyl use.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Fentanyl/pharmacology ; Humans ; Opiate Substitution Treatment/methods ; Opioid-Related Disorders/drug therapy ; Opioid-Related Disorders/epidemiology ; Receptors, Opioid, mu/agonists
Chemical Substances	Analgesics, Opioid ; Receptors, Opioid, mu ; Fentanyl (UF599785JZ)
Language	English
Publishing date	2018-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2018.12.005
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Zs.A 1371: Show issues

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Article ; Online: Pain Catastrophizing Is Associated With Increased Alcohol Cue-Elicited Neural Activity Among Individuals With Alcohol Use Disorder.

Nieto, Steven J / Grodin, Erica N / Burnette, Elizabeth M / Cahill, Catherine M / Ray, Lara A

Alcohol and alcoholism (Oxford, Oxfordshire)

2022 Volume 57, Issue 6, Page(s) 727–733

Abstract: Aims: The current study examined the association between pain catastrophizing and alcohol cue-elicited brain activation in individuals with alcohol use disorder (AUD).: Methods: Non-treatment seeking heavy drinkers with AUD (n = 45; 28 males) ... ...

Abstract	Aims: The current study examined the association between pain catastrophizing and alcohol cue-elicited brain activation in individuals with alcohol use disorder (AUD). Methods: Non-treatment seeking heavy drinkers with AUD (n = 45; 28 males) completed self-report measures of pain catastrophizing and alcohol use/problems as part of a clinical trial of the neuroimmune modulator ibudilast. Participants were randomized to either placebo (n = 25) or ibudilast (n = 20) and completed an functional magnetic resonance imaging (fMRI) scan to assess neural activation to alcohol cues 1 week into the medication trial. Multiple linear regression examined whether pain catastrophizing predicted cue-induced activation in a priori regions of interest, namely the dorsal and ventral striatum (VS). An exploratory whole-brain analysis was conducted to assess the relationship between pain catastrophizing and neural alcohol cue reactivity. Results: Pain catastrophizing predicted greater cue-induced activation in the dorsal (b = 0.006; P = 0.03) but not VS controlling for medication. Pain catastrophizing was positively associated with neural activation to alcohol cues in regions including the bilateral thalamus, left precuneus and left frontal pole. Conclusion: Greater pain catastrophizing is associated with greater cue-induced neural activation in brain regions sub-serving habits and compulsive alcohol use. These findings provide initial support for a neural mechanism by which pain catastrophizing may drive alcohol craving among individuals with AUD.
MeSH term(s)	Male ; Humans ; Alcoholism/drug therapy ; Cues ; Catastrophization ; Alcohol Drinking ; Craving/physiology ; Magnetic Resonance Imaging/methods ; Brain/physiology ; Ethanol
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2022-06-30
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	604956-4
ISSN	1464-3502 ; 0309-1635 ; 0735-0414
ISSN (online)	1464-3502
ISSN	0309-1635 ; 0735-0414
DOI	10.1093/alcalc/agac029
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Zs.B 798: Show issues

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Article ; Online: Neuroinflammation drives sex-dependent effects on pain and negative affect in a murine model of repeated mild traumatic brain injury.

Liu, Shiwei Steve / Pickens, Sarah / Barta, Zack / Rice, Myra / Dagher, Merel / Lebens, Ryan / Nguyen, Theodore V / Cummings, Brian J / Cahill, Catherine M

Pain

2023 Volume 165, Issue 4, Page(s) 848–865

Abstract: Abstract: The Center for Disease Control and Prevention estimates that 75% of reported cases of traumatic brain injury (TBI) are mild, where chronic pain and depression are 2 of the most common symptoms. In this study, we used a murine model of repeated ...

Abstract	Abstract: The Center for Disease Control and Prevention estimates that 75% of reported cases of traumatic brain injury (TBI) are mild, where chronic pain and depression are 2 of the most common symptoms. In this study, we used a murine model of repeated mild TBI to characterize the associated pain hypersensitivity and affective-like behavior and to what extent microglial reactivity contributes to these behavioral phenotypes. Male and female C57BL/6J mice underwent sham or repeated mild traumatic brain injury (rmTBI) and were tested for up to 9 weeks postinjury, where an anti-inflammatory/neuroprotective drug (minocycline) was introduced at 5 weeks postinjury in the drinking water. Repeated mild traumatic brain injury mice developed cold nociceptive hypersensitivity and negative affective states, as well as increased locomotor activity and risk-taking behavior. Minocycline reversed negative affect and pain hypersensitivities in male but not female mice. Repeated mild traumatic brain injury also produced an increase in microglial and brain-derived neurotropic factor mRNA transcripts in limbic structures known to be involved in nociception and affect, but many of these changes were sex dependent. Finally, we show that the antiepileptic drug, gabapentin, produced negative reinforcement in male rmTBI mice that was prevented by minocycline treatment, whereas rmTBI female mice showed a place aversion to gabapentin. Collectively, pain hypersensitivity, increased tonic-aversive pain components, and negative affective states were evident in both male and female rmTBI mice, but suppression of microglial reactivity was only sufficient to reverse behavioral changes in male mice. Neuroinflammation in limbic structures seems to be a contributing factor in behavioral changes resulting from rmTBI.
MeSH term(s)	Mice ; Male ; Female ; Animals ; Brain Concussion/complications ; Brain Concussion/psychology ; Neuroinflammatory Diseases ; Disease Models, Animal ; Minocycline/pharmacology ; Minocycline/therapeutic use ; Gabapentin ; Mice, Inbred C57BL ; Pain
Chemical Substances	Minocycline (FYY3R43WGO) ; Gabapentin (6CW7F3G59X)
Language	English
Publishing date	2023-11-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000003084
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Zs.A 1158: Show issues

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