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Article: Genetic mapping identifies Homer1 as a developmental modifier of attention.

Gershon, Zachary / Bonito-Oliva, Alessandra / Kanke, Matt / Terceros, Andrea / Rankin, Genelle / Fak, John / Harada, Yujin / Iannone, Andrew F / Gebremedhin, Millennium / Fabella, Brian / De Marco Garcia, Natalia V / Sethupathy, Praveen / Rajasethupathy, Priya

bioRxiv : the preprint server for biology

2024

Abstract: Attention is required for most higher-order cognitive functions. Prior studies have revealed functional roles for the prefrontal cortex and its extended circuits to enabling attention, but the underlying molecular processes and their impacts on cellular ... ...

Abstract	Attention is required for most higher-order cognitive functions. Prior studies have revealed functional roles for the prefrontal cortex and its extended circuits to enabling attention, but the underlying molecular processes and their impacts on cellular and circuit function remain poorly understood. To develop insights, we here took an unbiased forward genetics approach to identify single genes of large effect on attention. We studied 200 genetically diverse mice on measures of pre-attentive processing and through genetic mapping identified a small locus on chromosome 13 (95%CI: 92.22-94.09 Mb) driving substantial variation (19%) in this trait. Further characterization of the locus revealed a causative gene, Homer1, encoding a synaptic protein, where down-regulation of its short isoforms in prefrontal cortex (PFC) during early postnatal development led to improvements in multiple measures of attention in the adult. Subsequent mechanistic studies revealed that prefrontal
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.17.533136
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Article ; Online: Anteromedial thalamus gates the selection and stabilization of long-term memories.

Toader, Andrew C / Regalado, Josue M / Li, Yan Ran / Terceros, Andrea / Yadav, Nakul / Kumar, Suraj / Satow, Sloane / Hollunder, Florian / Bonito-Oliva, Alessandra / Rajasethupathy, Priya

Cell

2023 Volume 186, Issue 7, Page(s) 1369–1381.e17

Abstract: Memories initially formed in hippocampus gradually stabilize to cortex over weeks-to-months for long-term storage. The mechanistic details of this brain re-organization remain poorly understood. We recorded bulk neural activity in circuits that link ... ...

Abstract	Memories initially formed in hippocampus gradually stabilize to cortex over weeks-to-months for long-term storage. The mechanistic details of this brain re-organization remain poorly understood. We recorded bulk neural activity in circuits that link hippocampus and cortex as mice performed a memory-guided virtual-reality task over weeks. We identified a prominent and sustained neural correlate of memory in anterior thalamus, whose inhibition substantially disrupted memory consolidation. More strikingly, gain amplification enhanced consolidation of otherwise unconsolidated memories. To gain mechanistic insights, we developed a technology for simultaneous cellular-resolution imaging of hippocampus, thalamus, and cortex throughout consolidation. We found that whereas hippocampus equally encodes multiple memories, the anteromedial thalamus preferentially encodes salient memories, and gradually increases correlations with cortex to facilitate tuning and synchronization of cortical ensembles. We thus identify a thalamo-cortical circuit that gates memory consolidation and propose a mechanism suitable for the selection and stabilization of hippocampal memories into longer-term cortical storage.
MeSH term(s)	Mice ; Animals ; Memory, Long-Term/physiology ; Thalamus/physiology ; Hippocampus/physiology ; Memory Consolidation/physiology ; Brain
Language	English
Publishing date	2023-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.02.024
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Article: Anteromedial Thalamus Gates the Selection & Stabilization of Long-Term Memories.

Toader, Andrew C / Regalado, Josue M / Li, Yan Ran / Terceros, Andrea / Yadav, Nakul / Kumar, Suraj / Satow, Sloane / Hollunder, Florian / Bonito-Oliva, Alessandra / Rajasethupathy, Priya

bioRxiv : the preprint server for biology

2023

Abstract: Memories initially formed in hippocampus gradually stabilize to cortex, over weeks-to-months, for long-term storage. The mechanistic details of this brain re-organization process remain poorly understood. In this study, we developed a virtual-reality ... ...

Abstract	Memories initially formed in hippocampus gradually stabilize to cortex, over weeks-to-months, for long-term storage. The mechanistic details of this brain re-organization process remain poorly understood. In this study, we developed a virtual-reality based behavioral task and observed neural activity patterns associated with memory reorganization and stabilization over weeks-long timescales. Initial photometry recordings in circuits that link hippocampus and cortex revealed a unique and prominent neural correlate of memory in anterior thalamus that emerged in training and persisted for several weeks. Inhibition of the anteromedial thalamus-to-anterior cingulate cortex projections during training resulted in substantial memory consolidation deficits, and gain amplification more strikingly, was sufficient to enhance consolidation of otherwise unconsolidated memories. To provide mechanistic insights, we developed a new behavioral task where mice form two memories, of which only the more salient memory is consolidated, and also a technology for simultaneous and longitudinal cellular resolution imaging of hippocampus, thalamus, and cortex throughout the consolidation window. We found that whereas hippocampus equally encodes multiple memories, the anteromedial thalamus forms preferential tuning to salient memories, and establishes inter-regional correlations with cortex, that are critical for synchronizing and stabilizing cortical representations at remote time. Indeed, inhibition of this thalamo-cortical circuit while imaging in cortex reveals loss of contextual tuning and ensemble synchrony in anterior cingulate, together with behavioral deficits in remote memory retrieval. We thus identify a thalamo-cortical circuit that gates memory consolidation and propose a mechanism suitable for the selection and stabilization of hippocampal memories into longer term cortical storage.
Language	English
Publishing date	2023-01-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.27.525908
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Article ; Online: Update on Alzheimer's Disease Therapy and Prevention Strategies.

Graham, W Vallen / Bonito-Oliva, Alessandra / Sakmar, Thomas P

Annual review of medicine

2017 Volume 68, Page(s) 413–430

Abstract: Alzheimer's disease (AD) is the primary cause of age-related dementia. Effective strategies to prevent and treat AD remain elusive despite major efforts to understand its basic biology and clinical pathophysiology. Significant investments in therapeutic ... ...

Abstract	Alzheimer's disease (AD) is the primary cause of age-related dementia. Effective strategies to prevent and treat AD remain elusive despite major efforts to understand its basic biology and clinical pathophysiology. Significant investments in therapeutic drug discovery programs over the past two decades have yielded some important insights but no blockbuster drugs to alter the course of disease. Because significant memory loss and cognitive decline are associated with neuron death and loss of gray matter, especially in the frontal cortex and hippocampus, some focus in drug development has shifted to early prevention of cellular pathology. Although clinical trial design is challenging, due in part to a lack of robust biomarkers with predictive value, some optimism has come from the identification and study of inherited forms of early-onset AD and genetic risk factors that provide insights about molecular pathophysiology and potential drug targets. In addition, better understanding of the Aβ amyloid pathway and the tau pathway-leading to amyloid plaques and neurofibrillary tangles, respectively, which are histopathological hallmarks of AD-continues to drive significant drug research and development programs. The main focus of this review is to summarize the most recent basic biology, biochemistry, and pharmacology that serve as a foundation for more than 50 active advanced-phase clinical trials for AD prevention and therapy.
Language	English
Publishing date	2017-01-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	207930-6
ISSN	1545-326X ; 0066-4219
ISSN (online)	1545-326X
ISSN	0066-4219
DOI	10.1146/annurev-med-042915-103753
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Article: Inhibition of mTORC1 Signaling Reverts Cognitive and Affective Deficits in a Mouse Model of Parkinson's Disease.

Masini, Débora / Bonito-Oliva, Alessandra / Bertho, Maëlle / Fisone, Gilberto

Frontiers in neurology

2018 Volume 9, Page(s) 208

Abstract: Non-motor symptoms, including cognitive deficits and affective disorders, are frequently diagnosed in Parkinson's disease (PD) patients and are only partially alleviated by dopamine replacement therapy. Here, we used a 6-hydroxydopamine (6-OHDA) mouse ... ...

Abstract	Non-motor symptoms, including cognitive deficits and affective disorders, are frequently diagnosed in Parkinson's disease (PD) patients and are only partially alleviated by dopamine replacement therapy. Here, we used a 6-hydroxydopamine (6-OHDA) mouse model of PD to examine the effects exerted on non-motor symptoms by inhibition of the mammalian target of rapamycin complex 1 (mTORC1), which is involved in the control of protein synthesis, cell growth, and metabolism. We show that rapamycin, which acts as an allosteric inhibitor of mTORC1, counteracts the impairment of novel object recognition. A similar effect is produced by PF-4708671, an inhibitor of the downstream target of mTORC1, ribosomal protein S6 kinase (S6K). Rapamycin is also able to reduce depression-like behavior in PD mice, as indicated by decreased immobility in the forced swim test. Moreover, rapamycin exerts anxiolytic effects, thereby reducing thigmotaxis in the open field and increasing exploration of the open arm in the elevated plus maze. In contrast to rapamycin, administration of PF-4708671 to PD mice does not counteract depression- and anxiety-like behaviors. Altogether, these results identify mTORC1 as a target for the development of drugs that, in combination with standard antiparkinsonian agents, may widen the efficacy of current therapies for the cognitive and affective symptoms of PD.
Language	English
Publishing date	2018-04-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2018.00208
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Article ; Online: Anteromedial thalamus gates the selection and stabilization of long-term memories

Toader, Andrew C. / Regalado, Josue M. / Li, Yan Ran / Terceros, Andrea / Yadav, Nakul / Kumar, Suraj / Satow, Sloane / Hollunder, Florian / Bonito-Oliva, Alessandra / Rajasethupathy, Priya

Cell. 2023 Mar., v. 186, no. 7 p.1369-1381.e17

2023

Abstract	Memories initially formed in hippocampus gradually stabilize to cortex over weeks-to-months for long-term storage. The mechanistic details of this brain re-organization remain poorly understood. We recorded bulk neural activity in circuits that link hippocampus and cortex as mice performed a memory-guided virtual-reality task over weeks. We identified a prominent and sustained neural correlate of memory in anterior thalamus, whose inhibition substantially disrupted memory consolidation. More strikingly, gain amplification enhanced consolidation of otherwise unconsolidated memories. To gain mechanistic insights, we developed a technology for simultaneous cellular-resolution imaging of hippocampus, thalamus, and cortex throughout consolidation. We found that whereas hippocampus equally encodes multiple memories, the anteromedial thalamus preferentially encodes salient memories, and gradually increases correlations with cortex to facilitate tuning and synchronization of cortical ensembles. We thus identify a thalamo-cortical circuit that gates memory consolidation and propose a mechanism suitable for the selection and stabilization of hippocampal memories into longer-term cortical storage.
Keywords	cortex ; hippocampus ; memory ; storage time ; thalamus ; consolidation ; virtual-reality ; imaging ; optogenetics ; calcium imaging ; dynamics
Language	English
Dates of publication	2023-03
Size	p. 1369-1381.e17.
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.02.024
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Bonn / Germany

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Article ; Online: Human Islet Amyloid Polypeptide (hIAPP) Protofibril-Specific Antibodies for Detection and Treatment of Type 2 Diabetes.

Bortoletto, Angelina S / Graham, W Vallen / Trout, Gabriella / Bonito-Oliva, Alessandra / Kazmi, Manija A / Gong, Jing / Weyburne, Emily / Houser, Brandy L / Sakmar, Thomas P / Parchem, Ronald J

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2022 Volume 9, Issue 34, Page(s) e2202342

Abstract: Type 2 diabetes mellitus (T2D) is a major public health concern and is characterized by sustained hyperglycemia due to insulin resistance and destruction of insulin-producing β cells. One pathological hallmark of T2D is the toxic accumulation of human ... ...

Abstract	Type 2 diabetes mellitus (T2D) is a major public health concern and is characterized by sustained hyperglycemia due to insulin resistance and destruction of insulin-producing β cells. One pathological hallmark of T2D is the toxic accumulation of human islet amyloid polypeptide (hIAPP) aggregates. Monomeric hIAPP is a hormone normally co-secreted with insulin. However, increased levels of hIAPP in prediabetic and diabetic patients can lead to the formation of hIAPP protofibrils, which are toxic to β cells. Current therapies fail to address hIAPP aggregation and current screening modalities do not detect it. Using a stabilizing capping protein, monoclonal antibodies (mAbs) can be developed against a previously nonisolatable form of hIAPP protofibrils, which are protofibril specific and do not engage monomeric hIAPP. Shown here are two candidate mAbs that can detect hIAPP protofibrils in serum and hIAPP deposits in pancreatic islets in a mouse model of rapidly progressing T2D. Treatment of diabetic mice with the mAbs delays disease progression and dramatically increases overall survival. These results demonstrate the potential for using novel hIAPP protofibril-specific mAbs as a diagnostic screening tool for early detection of T2D, as well as therapeutically to preserve β cell function and target one of the underlying pathological mechanisms of T2D.
MeSH term(s)	Humans ; Mice ; Animals ; Diabetes Mellitus, Type 2/diagnosis ; Diabetes Mellitus, Type 2/therapy ; Islet Amyloid Polypeptide ; Diabetes Mellitus, Experimental ; Personality ; Insulin
Chemical Substances	Islet Amyloid Polypeptide ; Insulin
Language	English
Publishing date	2022-10-18
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202202342
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Article ; Online: Nucleobindin 1 binds to multiple types of pre-fibrillar amyloid and inhibits fibrillization.

Bonito-Oliva, Alessandra / Barbash, Shahar / Sakmar, Thomas P / Graham, W Vallen

Scientific reports

2017 Volume 7, Page(s) 42880

Abstract: During amyloid fibril formation, amyloidogenic polypeptides misfold and self assemble into soluble pre-fibrillar aggregates, i.e., protofibrils, which elongate and mature into insoluble fibrillar aggregates. An emerging class of chaperones, chaperone- ... ...

Abstract	During amyloid fibril formation, amyloidogenic polypeptides misfold and self assemble into soluble pre-fibrillar aggregates, i.e., protofibrils, which elongate and mature into insoluble fibrillar aggregates. An emerging class of chaperones, chaperone-like amyloid binding proteins (CLABPs), has been shown to interfere with aggregation of particular misfolded amyloid peptides or proteins. We have discovered that the calcium-binding protein nuclebindin-1 (NUCB1) is a novel CLABP. We show that NUCB1 inhibits aggregation of islet-amyloid polypeptide associated with type 2 diabetes mellitus, a-synuclein associated with Parkinson's disease, transthyretin V30M mutant associated with familial amyloid polyneuropathy, and Aβ42 associated with Alzheimer's disease by stabilizing their respective protofibril intermediates. Kinetic studies employing the modeling software AmyloFit show that NUCB1 affects both primary nucleation and secondary nucleation. We hypothesize that NUCB1 binds to the common cross-β-sheet structure of protofibril aggregates to "cap" and stabilize soluble macromolecular complexes. Transmission electron microscopy and atomic force microscopy were employed to characterize the size, shape and volume distribution of multiple sources of NUCB1-capped protofibrils. Interestingly, NUCB1 prevents Aβ42 protofibril toxicity in a cellular assay. NUCB1-stabilized amyloid protofibrils could be used as immunogens to prepare conformation-specific antibodies and as novel tools to develop screens for anti-protofibril diagnostics and therapeutics.
MeSH term(s)	Amyloid/chemistry ; Amyloid/metabolism ; Amyloid beta-Peptides/chemistry ; Amyloid beta-Peptides/metabolism ; Calcium-Binding Proteins/chemistry ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Humans ; Islet Amyloid Polypeptide/chemistry ; Islet Amyloid Polypeptide/metabolism ; Kinetics ; Microscopy, Atomic Force ; Mutagenesis, Site-Directed ; Nerve Tissue Proteins/chemistry ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Peptide Fragments/chemistry ; Peptide Fragments/metabolism ; Prealbumin/chemistry ; Prealbumin/metabolism ; Protein Binding ; Protein Structure, Secondary ; alpha-Synuclein/chemistry ; alpha-Synuclein/metabolism
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Calcium-Binding Proteins ; DNA-Binding Proteins ; Islet Amyloid Polypeptide ; Nerve Tissue Proteins ; Peptide Fragments ; Prealbumin ; alpha-Synuclein ; amyloid beta-protein (1-42) ; nucleobindin ; amyloid prealbumin (87090-18-4)
Language	English
Publishing date	2017-02-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep42880
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Article: A mouse model of non-motor symptoms in Parkinson's disease: focus on pharmacological interventions targeting affective dysfunctions.

Bonito-Oliva, Alessandra / Masini, Débora / Fisone, Gilberto

Frontiers in behavioral neuroscience

2014 Volume 8, Page(s) 290

Abstract: Non-motor symptoms, including psychiatric disorders, are increasingly recognized as a major challenge in the treatment of Parkinson's disease (PD). These ailments, which often appear in the early stage of the disease, affect a large number of patients ... ...

Abstract	Non-motor symptoms, including psychiatric disorders, are increasingly recognized as a major challenge in the treatment of Parkinson's disease (PD). These ailments, which often appear in the early stage of the disease, affect a large number of patients and are only partly resolved by conventional antiparkinsonian medications, such as L-DOPA. Here, we investigated non-motor symptoms of PD in a mouse model based on bilateral injection of the toxin 6-hydroxydopamine (6-OHDA) in the dorsal striatum. This model presented only subtle gait modifications, which did not affect horizontal motor activity in the open-field test. Bilateral 6-OHDA lesion also impaired olfactory discrimination, in line with the anosmia typically observed in early stage parkinsonism. The effect of 6-OHDA was then examined for mood-related dysfunctions. Lesioned mice showed increased immobility in the forced swim test and tail suspension test, two behavioral paradigms of depression. Moreover, the lesion exerted anxiogenic effects, as shown by reduced time spent in the open arms, in the elevated plus maze test, and by increased thigmotaxis in the open-field test. L-DOPA did not modify depressive- and anxiety-like behaviors, which were instead counteracted by the dopamine D2/D3 receptor agonist, pramipexole. Reboxetine, a noradrenaline reuptake inhibitor, was also able to revert the depressive and anxiogenic effects produced by the lesion with 6-OHDA. Interestingly, pre-treatment with desipramine prior to injection of 6-OHDA, which is commonly used to preserve noradrenaline neurons, did not modify the effect of the lesion on depressive- and anxiety-like behaviors. Thus, in the present model, mood-related conditions are independent of the reduction of noradrenaline caused by 6-OHDA. Based on these findings we propose that the anti-depressive and anxiolytic action of reboxetine is mediated by promoting dopamine transmission through blockade of dopamine uptake from residual noradrenergic terminals.
Language	English
Publishing date	2014-08-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452960-6
ISSN	1662-5153
ISSN	1662-5153
DOI	10.3389/fnbeh.2014.00290
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Article ; Online: Atypical but not typical antipsychotic drugs ameliorate phencyclidine-induced emotional memory impairments in mice.

Adem, Abdu / Madjid, Nather / Stiedl, Oliver / Bonito-Oliva, Alessandra / Konradsson-Geuken, Åsa / Holst, Sarah / Fisone, Gilberto / Ögren, Sven Ove

European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology

2019 Volume 29, Issue 5, Page(s) 616–628

Abstract: Schizophrenia is associated with cognitive impairments related to hypofunction in glutamatergic N-methyl-D-aspartate receptor (NMDAR) transmission. Phencyclidine (PCP), a non-competitive NMDAR antagonist, models schizophrenia-like behavioral symptoms ... ...

Abstract	Schizophrenia is associated with cognitive impairments related to hypofunction in glutamatergic N-methyl-D-aspartate receptor (NMDAR) transmission. Phencyclidine (PCP), a non-competitive NMDAR antagonist, models schizophrenia-like behavioral symptoms including cognitive deficits in rodents. This study examined the effects of PCP on emotional memory function examined in the passive avoidance (PA) task in mice and the ability of typical and atypical antipsychotic drugs (APDs) to rectify the PCP-mediated impairment. Pre-training administration of PCP (0.5, 1, 2 or 3 mg/kg) dose-dependently interfered with memory consolidation in the PA task. In contrast, PCP was ineffective when administered after training, and immediately before the retention test indicating that NMDAR blockade interferes with memory encoding mechanisms. The typical APD haloperidol and the dopamine D
MeSH term(s)	Animals ; Antipsychotic Agents/pharmacology ; Antipsychotic Agents/therapeutic use ; Clozapine/pharmacology ; Clozapine/therapeutic use ; Dose-Response Relationship, Drug ; Emotional Regulation/drug effects ; Emotional Regulation/physiology ; Excitatory Amino Acid Antagonists/toxicity ; Haloperidol/pharmacology ; Haloperidol/therapeutic use ; Male ; Memory Disorders/chemically induced ; Memory Disorders/drug therapy ; Memory Disorders/psychology ; Mice ; Mice, Inbred C57BL ; Phencyclidine/toxicity ; Serotonin 5-HT1 Receptor Antagonists/pharmacology ; Serotonin 5-HT1 Receptor Antagonists/therapeutic use
Chemical Substances	Antipsychotic Agents ; Excitatory Amino Acid Antagonists ; Serotonin 5-HT1 Receptor Antagonists ; Phencyclidine (J1DOI7UV76) ; Clozapine (J60AR2IKIC) ; Haloperidol (J6292F8L3D)
Language	English
Publishing date	2019-03-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1082947-7
ISSN	1873-7862 ; 0924-977X
ISSN (online)	1873-7862
ISSN	0924-977X
DOI	10.1016/j.euroneuro.2019.03.007
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Zs.MO 630: Show issues

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