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Article ; Online: Playing With Objects Engages Brain Reward System and Counteracts Stress-Induced Depressive-like Behavior.

Puglisi-Allegra, Stefano

2022 Volume 91, Issue 7, Page(s) 612–614

MeSH term(s)	Brain ; Reward
Language	English
Publishing date	2022-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2022.01.001
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Article ; Online: Autophagy status as a gateway for stress-induced catecholamine interplay in neurodegeneration.

Fornai, Francesco / Puglisi-Allegra, Stefano

Neuroscience and biobehavioral reviews

2021 Volume 123, Page(s) 238–256

Abstract: The catecholamine-containing brainstem nuclei locus coeruleus (LC) and ventral tegmental area (VTA) are critically involved in stress responses. Alterations of catecholamine systems during chronic stress may contribute to neurodegeneration, including ... ...

Abstract	The catecholamine-containing brainstem nuclei locus coeruleus (LC) and ventral tegmental area (VTA) are critically involved in stress responses. Alterations of catecholamine systems during chronic stress may contribute to neurodegeneration, including cognitive decline. Stress-related catecholamine alterations, while contributing to anxiety and depression, might accelerate neuronal degeneration by increasing the formation of toxic dopamine and norepinephrine by-products. These, in turn, may impair proteostasis within a variety of cortical and subcortical areas. In particular, the molecular events governing neurotransmission, neuroplasticity, and proteostasis within LC and VTA affect a variety of brain areas. Therefore, we focus on alterations of autophagy machinery in these nuclei as a relevant trigger in this chain of events. In fact, these catecholamine-containing areas are mostly prone to autophagy-dependent neurodegeneration. Thus, we propose a dynamic hypothesis according to which stress-induced autophagy alterations within the LC-VTA network foster a cascade towards early neurodegeneration within these nuclei.
MeSH term(s)	Autophagy ; Catecholamines ; Humans ; Locus Coeruleus ; Norepinephrine ; Ventral Tegmental Area
Chemical Substances	Catecholamines ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2021-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2021.01.015
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Article ; Online: Translational evidence for lithium-induced brain plasticity and neuroprotection in the treatment of neuropsychiatric disorders.

Puglisi-Allegra, Stefano / Ruggieri, Stefano / Fornai, Francesco

Translational psychiatry

2021 Volume 11, Issue 1, Page(s) 366

Abstract: Increasing evidence indicates lithium ( ... ...

Abstract	Increasing evidence indicates lithium (Li
MeSH term(s)	Antimanic Agents/therapeutic use ; Bipolar Disorder/drug therapy ; Humans ; Lithium/therapeutic use ; Lithium Compounds/pharmacology ; Neuronal Plasticity ; Neuroprotection
Chemical Substances	Antimanic Agents ; Lithium Compounds ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2021-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-021-01492-7
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Article: Prefrontal Dopamine in Flexible Adaptation to Environmental Changes: A Game for Two Players.

Latagliata, Emanuele Claudio / Orsini, Cristina / Cabib, Simona / Biagioni, Francesca / Fornai, Francesco / Puglisi-Allegra, Stefano

Biomedicines

2023 Volume 11, Issue 12

Abstract: Deficits in cognitive flexibility have been characterized in affective, anxiety, and neurodegenerative disorders. This paper reviews data, mainly from studies on animal models, that support the existence of a cortical-striatal brain circuit modulated by ... ...

Abstract	Deficits in cognitive flexibility have been characterized in affective, anxiety, and neurodegenerative disorders. This paper reviews data, mainly from studies on animal models, that support the existence of a cortical-striatal brain circuit modulated by dopamine (DA), playing a major role in cognitive/behavioral flexibility. Moreover, we reviewed clinical findings supporting misfunctioning of this circuit in Parkinson's disease that could be responsible for some important non-motoric symptoms. The reviewed findings point to a role of catecholaminergic transmission in the medial prefrontal cortex (mpFC) in modulating DA's availability in the nucleus accumbens (NAc), as well as a role of NAc DA in modulating the motivational value of natural and conditioned stimuli. The review section is accompanied by a preliminary experiment aimed at testing weather the extinction of a simple Pavlovian association fosters increased DA transmission in the mpFC and inhibition of DA transmission in the NAc.
Language	English
Publishing date	2023-11-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11123189
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Article ; Online: Lithium engages autophagy for neuroprotection and neuroplasticity: Translational evidence for therapy.

Puglisi-Allegra, Stefano / Lazzeri, Gloria / Busceti, Carla L / Giorgi, Filippo S / Biagioni, Francesca / Fornai, Francesco

Neuroscience and biobehavioral reviews

2023 Volume 148, Page(s) 105148

Abstract: Here an overview is provided on therapeutic/neuroprotective effects of Lithifum ( ... ...

Abstract	Here an overview is provided on therapeutic/neuroprotective effects of Lithifum (Li
MeSH term(s)	Humans ; Neuroprotection ; Lithium/pharmacology ; Lithium/therapeutic use ; Neurodegenerative Diseases/drug therapy ; Autophagy ; Neuronal Plasticity
Chemical Substances	Lithium (9FN79X2M3F)
Language	English
Publishing date	2023-03-28
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2023.105148
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Article ; Online: Damage to the Locus Coeruleus Alters the Expression of Key Proteins in Limbic Neurodegeneration.

Biagioni, Francesca / Ferrucci, Michela / Lazzeri, Gloria / Scioli, Mariarosaria / Frati, Alessandro / Puglisi-Allegra, Stefano / Fornai, Francesco

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: The present investigation was designed based on the evidence that, in neurodegenerative disorders, such as Alzheimer's dementia (AD) and Parkinson's disease (PD), damage to the locus coeruleus (LC) arising norepinephrine (NE) axons (LC-NE) is documented ... ...

Abstract	The present investigation was designed based on the evidence that, in neurodegenerative disorders, such as Alzheimer's dementia (AD) and Parkinson's disease (PD), damage to the locus coeruleus (LC) arising norepinephrine (NE) axons (LC-NE) is documented and hypothesized to foster the onset and progression of neurodegeneration within target regions. Specifically, the present experiments were designed to assess whether selective damage to LC-NE axons may alter key proteins involved in neurodegeneration within specific limbic regions, such as the hippocampus and piriform cortex, compared with the dorsal striatum. To achieve this, a loss of LC-NE axons was induced by the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) in C57 Black mice, as assessed by a loss of NE and dopamine-beta-hydroxylase within target regions. In these experimental conditions, the amount of alpha-synuclein (alpha-syn) protein levels were increased along with alpha-syn expressing neurons within the hippocampus and piriform cortex. Similar findings were obtained concerning phospho-Tau immunoblotting. In contrast, a decrease in inducible HSP70-expressing neurons and a loss of sequestosome (p62)-expressing cells, along with a loss of these proteins at immunoblotting, were reported. The present data provide further evidence to understand why a loss of LC-NE axons may foster limbic neurodegeneration in AD and limbic engagement during PD.
MeSH term(s)	Mice ; Animals ; Locus Coeruleus/metabolism ; Norepinephrine/metabolism ; Neurons/metabolism ; Neurotoxins/pharmacology ; Axons/metabolism ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Parkinson Disease/metabolism
Chemical Substances	Norepinephrine (X4W3ENH1CV) ; Neurotoxins
Language	English
Publishing date	2024-03-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25063159
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Article ; Online: Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.

Lenzi, Paola / Lazzeri, Gloria / Ferrucci, Michela / Scotto, Marco / Frati, Alessandro / Puglisi-Allegra, Stefano / Busceti, Carla Letizia / Fornai, Francesco

International journal of molecular sciences

2024 Volume 25, Issue 7

Abstract: In the last two decades, alpha-synuclein (alpha-syn) assumed a prominent role as a major component and seeding structure of Lewy bodies (LBs). This concept is driving ongoing research on the pathophysiology of Parkinson's disease (PD). In line with this, ...

Abstract	In the last two decades, alpha-synuclein (alpha-syn) assumed a prominent role as a major component and seeding structure of Lewy bodies (LBs). This concept is driving ongoing research on the pathophysiology of Parkinson's disease (PD). In line with this, alpha-syn is considered to be the guilty protein in the disease process, and it may be targeted through precision medicine to modify disease progression. Therefore, designing specific tools to block the aggregation and spreading of alpha-syn represents a major effort in the development of disease-modifying therapies in PD. The present article analyzes concrete evidence about the significance of alpha-syn within LBs. In this effort, some dogmas are challenged. This concerns the question of whether alpha-syn is more abundant compared with other proteins within LBs. Again, the occurrence of alpha-syn compared with non-protein constituents is scrutinized. Finally, the prominent role of alpha-syn in seeding LBs as the guilty structure causing PD is questioned. These revisited concepts may be helpful in the process of validating which proteins, organelles, and pathways are likely to be involved in the damage to meso-striatal dopamine neurons and other brain regions involved in PD.
MeSH term(s)	Humans ; alpha-Synuclein ; Lewy Bodies ; Parkinson Disease ; Corpus Striatum ; Disease Progression
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2024-04-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25073929
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Article ; Online: Combined light and electron microscopy (CLEM) to quantify methamphetamine-induced alpha-synuclein-related pathology.

Ferrucci, Michela / Lenzi, Paola / Lazzeri, Gloria / Busceti, Carla L / Frati, Alessandro / Puglisi-Allegra, Stefano / Fornai, Francesco

Journal of neural transmission (Vienna, Austria : 1996)

2024 Volume 131, Issue 4, Page(s) 335–358

Abstract: Methamphetamine (METH) produces a cytopathology, which is rather specific within catecholamine neurons both in vitro and ex vivo, in animal models and chronic METH abusers. This led some authors to postulate a sort of parallelism between METH ... ...

Abstract	Methamphetamine (METH) produces a cytopathology, which is rather specific within catecholamine neurons both in vitro and ex vivo, in animal models and chronic METH abusers. This led some authors to postulate a sort of parallelism between METH cytopathology and cell damage in Parkinson's disease (PD). In fact, METH increases and aggregates alpha-syn proto-fibrils along with producing spreading of alpha-syn. Although alpha-syn is considered to be the major component of aggregates and inclusions developing within diseased catecholamine neurons including classic Lewy body (LB), at present, no study provided a quantitative assessment of this protein in situ, neither following METH nor in LB occurring in PD. Similarly, no study addressed the quantitative comparison between occurrence of alpha-syn and other key proteins and no investigation measured the protein compared with non-protein structure within catecholamine cytopathology. Therefore, the present study addresses these issues using an oversimplified model consisting of a catecholamine cell line where the novel approach of combined light and electron microscopy (CLEM) was used measuring the amount of alpha-syn, which is lower compared with p62 or poly-ubiquitin within pathological cell domains. The scenario provided by electron microscopy reveals unexpected findings, which are similar to those recently described in the pathology of PD featuring packing of autophagosome-like vesicles and key proteins shuttling autophagy substrates. Remarkably, small seed-like areas, densely packed with p62 molecules attached to poly-ubiquitin within wide vesicular domains occurred. The present data shed new light about quantitative morphometry of catecholamine cell damage in PD and within the addicted brain.
MeSH term(s)	Animals ; Methamphetamine/pharmacology ; alpha-Synuclein/metabolism ; Parkinson Disease/metabolism ; Microscopy, Electron ; Catecholamines ; Ubiquitins
Chemical Substances	Methamphetamine (44RAL3456C) ; alpha-Synuclein ; Catecholamines ; Ubiquitins
Language	English
Publishing date	2024-02-17
Publishing country	Austria
Document type	Journal Article ; 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/s00702-024-02741-x
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Article ; Online: Noradrenaline and Seizures: A Perspective on the Role of Adrenergic Receptors in Limbic Seizures.

Biagioni, Francesca / Celli, Roberta / Puglisi-Allegra, Stefano / Nicoletti, Ferdinando / Giorgi, Filippo Sean / Fornai, Francesco

Current neuropharmacology

2022 Volume 21, Issue 11, Page(s) 2233–2236

Abstract: Background: Noradrenergic fibers originating from the locus coeruleus densely innervate limbic structures, including the piriform cortex, which is the limbic structure with the lowest seizure threshold. Noradrenaline (NA) modulates limbic seizures while ...

Abstract	Background: Noradrenergic fibers originating from the locus coeruleus densely innervate limbic structures, including the piriform cortex, which is the limbic structure with the lowest seizure threshold. Noradrenaline (NA) modulates limbic seizures while stimulating autophagy through β Objective: In this perspective, we analyzed a potential role for β Methods: We developed this perspective based on current literature on the role of NA in limbic seizures and autophagy. The perspective is also grounded on preliminary data obtained by microinfusing within AT either a β Results: β Conclusion: NA counteracts limbic seizures. This relies on various receptors in different brain areas. The anterior piriform cortex plays a key role in patients affected by limbic epilepsy. The anticonvulsant effects of NA through β
MeSH term(s)	Rats ; Animals ; Humans ; Norepinephrine/adverse effects ; Norepinephrine/metabolism ; Bicuculline/adverse effects ; Anticonvulsants ; Rats, Sprague-Dawley ; Seizures/drug therapy ; Seizures/chemically induced ; Receptors, Adrenergic
Chemical Substances	Norepinephrine (X4W3ENH1CV) ; Bicuculline (Y37615DVKC) ; Anticonvulsants ; Receptors, Adrenergic
Language	English
Publishing date	2022-03-26
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2192352-8
ISSN	1875-6190 ; 1570-159X
ISSN (online)	1875-6190
ISSN	1570-159X
DOI	10.2174/1570159X20666220327213615
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Article ; Online: The Relevance of Autophagy within Inner Ear in Baseline Conditions and Tinnitus-Related Syndromes.

Lazzeri, Gloria / Biagioni, Francesca / Ferrucci, Michela / Puglisi-Allegra, Stefano / Lenzi, Paola / Busceti, Carla Letizia / Giannessi, Francesco / Fornai, Francesco

International journal of molecular sciences

2023 Volume 24, Issue 23

Abstract: Tinnitus is the perception of noise in the absence of acoustic stimulation (phantom noise). In most patients suffering from chronic peripheral tinnitus, an alteration of outer hair cells (OHC) starting from the stereocilia (SC) occurs. This is common ... ...

Abstract	Tinnitus is the perception of noise in the absence of acoustic stimulation (phantom noise). In most patients suffering from chronic peripheral tinnitus, an alteration of outer hair cells (OHC) starting from the stereocilia (SC) occurs. This is common following ototoxic drugs, sound-induced ototoxicity, and acoustic degeneration. In all these conditions, altered coupling between the tectorial membrane (TM) and OHC SC is described. The present review analyzes the complex interactions involving OHC and TM. These need to be clarified to understand which mechanisms may underlie the onset of tinnitus and why the neuropathology of chronic degenerative tinnitus is similar, independent of early triggers. In fact, the fine neuropathology of tinnitus features altered mechanisms of mechanic-electrical transduction (MET) at the level of OHC SC. The appropriate coupling between OHC SC and TM strongly depends on autophagy. The involvement of autophagy may encompass degenerative and genetic tinnitus, as well as ototoxic drugs and acoustic trauma. Defective autophagy explains mitochondrial alterations and altered protein handling within OHC and TM. This is relevant for developing novel treatments that stimulate autophagy without carrying the burden of severe side effects. Specific phytochemicals, such as curcumin and berberin, acting as autophagy activators, may mitigate the neuropathology of tinnitus.
MeSH term(s)	Humans ; Tinnitus ; Hair Cells, Auditory, Outer ; Stereocilia ; Sound ; Acoustic Stimulation
Language	English
Publishing date	2023-11-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242316664
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