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Article ; Online: Innovative pathological network-based multitarget approaches for Alzheimer's disease treatment.

Mayo, Paloma / Pascual, Jorge / Crisman, Enrique / Domínguez, Cristina / López, Manuela G / León, Rafael

2024

Abstract: Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and is a major health threat globally. Its prevalence is forecasted to exponentially increase during the next 30 years due to the global aging population. Currently, approved drugs ... ...

Abstract	Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and is a major health threat globally. Its prevalence is forecasted to exponentially increase during the next 30 years due to the global aging population. Currently, approved drugs are merely symptomatic, being ineffective in delaying or blocking the relentless disease advance. Intensive AD research describes this disease as a highly complex multifactorial disease. Disclosure of novel pathological pathways and their interconnections has had a major impact on medicinal chemistry drug development for AD over the last two decades. The complex network of pathological events involved in the onset of the disease has prompted the development of multitarget drugs. These chemical entities combine pharmacological activities toward two or more drug targets of interest. These multitarget-directed ligands are proposed to modify different nodes in the pathological network aiming to delay or even stop disease progression. Here, we review the multitarget drug development strategy for AD during the last decade.
Language	English
Publishing date	2024-04-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603210-2
ISSN	1098-1128 ; 0198-6325
ISSN (online)	1098-1128
ISSN	0198-6325
DOI	10.1002/med.22045
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Article ; Online: Cytotoxicity Models in Chromaffin Cells to Evaluate Neuroprotective Compounds.

Cano-Abad, María F / López, Manuela G

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2565, Page(s) 361–370

Abstract: Primary cultures of bovine chromaffin cells are considered a good model to evaluate potential neuroprotective compounds for two major reasons: (i) they share many common features to neurons as they synthesize, store, and release neurotransmitters; they ... ...

Abstract	Primary cultures of bovine chromaffin cells are considered a good model to evaluate potential neuroprotective compounds for two major reasons: (i) they share many common features to neurons as they synthesize, store, and release neurotransmitters; they are excitable cells that express voltage-dependent calcium, potassium, and sodium channels; they express different neuronal receptor subtypes; and (ii) they can be easily cultured in high quantities from adult animals; as adult para-neurons, they can be used to reproduce different neurodegenerative-like cytotoxicity models. In this chapter, we describe protocols to mimic calcium overload (veratridine and thapsigargin) and oxidative stress (rotenone plus oligomycin-A and 6-hydroxydopamine) to evaluate potential neuroprotective compounds.
MeSH term(s)	Animals ; Calcium/metabolism ; Cattle ; Cells, Cultured ; Chromaffin Cells/metabolism ; Neuroprotective Agents/pharmacology ; Neurotransmitter Agents ; Oligomycins ; Oxidopamine ; Potassium ; Rotenone ; Sodium Channels ; Thapsigargin ; Veratridine
Chemical Substances	Neuroprotective Agents ; Neurotransmitter Agents ; Oligomycins ; Sodium Channels ; Rotenone (03L9OT429T) ; Thapsigargin (67526-95-8) ; Veratridine (71-62-5) ; Oxidopamine (8HW4YBZ748) ; Potassium (RWP5GA015D) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-10-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2671-9_24
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Article ; Online: Central Activation of Alpha7 Nicotinic Signaling Attenuates LPS-Induced Neuroinflammation and Sickness Behavior in Adult but Not in Aged Animals.

Navarro, Elisa / Norden, Diana M / Trojanowski, Paige J / Godbout, Jonathan P / López, Manuela G

Molecules (Basel, Switzerland)

2021 Volume 26, Issue 8

Abstract: We previously reported that lipopolysaccharide (LPS) challenge caused microglial-mediated neuroinflammation and sickness behavior that was amplified in aged mice. As α7 nAChRs are implicated in the "Cholinergic anti-inflammatory pathway", we aimed to ... ...

Abstract	We previously reported that lipopolysaccharide (LPS) challenge caused microglial-mediated neuroinflammation and sickness behavior that was amplified in aged mice. As α7 nAChRs are implicated in the "Cholinergic anti-inflammatory pathway", we aimed to determine how α7 nAChR stimulation modulates microglial phenotype in an LPS-induced neuroinflammation model in adult and aged mice. For this, BALB/c mice were injected intraperitoneally with LPS (0.33 mg/kg) and treated with the α7 nAChR agonist PNU282987, using different administration protocols. LPS challenge reduced body weight and induced lethargy and social withdrawal in adult mice. Peripheral (intraperitoneal) co-administration of the α7 nAChR agonist PNU282987 with LPS, attenuated body weight loss and sickness behavior associated with LPS challenge in adult mice, and reduced microglial activation with suppression of IL-1β and TNFα mRNA levels. Furthermore, central (intracerebroventricular) administration of the α7 nAChR agonist, even 2 h after LPS injection, attenuated the decrease in social exploratory behavior and microglial activation induced by peripheral administration of LPS, although this recovery was not achieved if activation of α7 nAChRs was performed peripherally. Finally, we observed that the positive results of central activation of α7 nAChRs were lost in aged mice. In conclusion, we provide evidence that stimulation of α7 nAChR signaling reduces microglial activation in an in vivo LPS-based model, but this cholinergic-dependent regulation seems to be dysfunctional in microglia of aged mice.
MeSH term(s)	Age Factors ; Animals ; Behavior, Animal/drug effects ; Benzamides/pharmacology ; Bridged Bicyclo Compounds/pharmacology ; Central Nervous System Diseases/etiology ; Central Nervous System Diseases/metabolism ; Central Nervous System Diseases/physiopathology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Susceptibility ; Illness Behavior/drug effects ; Inflammation/etiology ; Inflammation/metabolism ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Lipopolysaccharides/adverse effects ; Mice ; Nicotinic Agonists/pharmacology ; Signal Transduction/drug effects ; alpha7 Nicotinic Acetylcholine Receptor/agonists ; alpha7 Nicotinic Acetylcholine Receptor/metabolism
Chemical Substances	Benzamides ; Bridged Bicyclo Compounds ; Cytokines ; Inflammation Mediators ; Lipopolysaccharides ; Nicotinic Agonists ; PNU-282987 ; alpha7 Nicotinic Acetylcholine Receptor
Language	English
Publishing date	2021-04-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules26082107
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Article ; Online: KEAP1-NRF2 protein-protein interaction inhibitors: Design, pharmacological properties and therapeutic potential.

Crisman, Enrique / Duarte, Pablo / Dauden, Esteban / Cuadrado, Antonio / Rodríguez-Franco, María Isabel / López, Manuela G / León, Rafael

Medicinal research reviews

2022 Volume 43, Issue 1, Page(s) 237–287

Abstract: The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is considered the master regulator of the phase II antioxidant response. It controls a plethora of cytoprotective genes related to oxidative stress, inflammation, and protein ... ...

Abstract	The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is considered the master regulator of the phase II antioxidant response. It controls a plethora of cytoprotective genes related to oxidative stress, inflammation, and protein homeostasis, among other processes. Activation of these pathways has been described in numerous pathologies including cancer, cardiovascular, respiratory, renal, digestive, metabolic, autoimmune, and neurodegenerative diseases. Considering the increasing interest of discovering novel NRF2 activators due to its clinical application, initial efforts were devoted to the development of electrophilic drugs able to induce NRF2 nuclear accumulation by targeting its natural repressor protein Kelch-like ECH-associated protein 1 (KEAP1) through covalent modifications on cysteine residues. However, off-target effects of these drugs prompted the development of an innovative strategy, the search of KEAP1-NRF2 protein-protein interaction (PPI) inhibitors. These innovative activators are proposed to target NRF2 in a more selective way, leading to potentially improved drugs with the application for a variety of diseases that are currently under investigation. In this review, we summarize known KEAP1-NRF2 PPI inhibitors to date and the bases of their design highlighting the most important features of their respective interactions. We also discuss the preclinical pharmacological properties described for the most promising compounds.
MeSH term(s)	Humans ; Inflammation/drug therapy ; Kelch-Like ECH-Associated Protein 1/antagonists & inhibitors ; Kelch-Like ECH-Associated Protein 1/metabolism ; Neurodegenerative Diseases ; NF-E2-Related Factor 2/antagonists & inhibitors ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress
Chemical Substances	KEAP1 protein, human ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2
Language	English
Publishing date	2022-09-10
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	603210-2
ISSN	1098-1128 ; 0198-6325
ISSN (online)	1098-1128
ISSN	0198-6325
DOI	10.1002/med.21925
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Zs.A 1764: Show issues

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Article: Aging and Progression of Beta-Amyloid Pathology in Alzheimer's Disease Correlates with Microglial Heme-Oxygenase-1 Overexpression.

Fernández-Mendívil, Cristina / Arreola, Miguel A / Hohsfield, Lindsay A / Green, Kim N / Lopez, Manuela G

Antioxidants (Basel, Switzerland)

2020 Volume 9, Issue 7

Abstract: Neuroinflammation and oxidative stress are being recognized as characteristic hallmarks in many neurodegenerative diseases, especially those that portray proteinopathy, such as Alzheimer's disease (AD). Heme-oxygenase 1 (HO-1) is an inducible enzyme with ...

Abstract	Neuroinflammation and oxidative stress are being recognized as characteristic hallmarks in many neurodegenerative diseases, especially those that portray proteinopathy, such as Alzheimer's disease (AD). Heme-oxygenase 1 (HO-1) is an inducible enzyme with antioxidant and anti-inflammatory properties, while microglia are the immune cells in the central nervous system. To elucidate the brain expression profile of microglial HO-1 in aging and AD-progression, we have used the 5xFAD (five familial AD mutations) mouse model of AD and their littermates at different ages (four, eight, 12, and 18 months). Total brain expression of HO-1 was increased with aging and such increase was even higher in 5xFAD animals. In co-localization studies, HO-1 expression was mainly found in microglia vs. other brain cells. The percentage of microglial cells expressing HO-1 and the amount of HO-1 expressed within microglia increased progressively with aging. Furthermore, this upregulation was increased by 2-3-fold in the elder 5xFAD mice. In addition, microglia overexpressing HO-1 was predominately found surrounding beta-amyloid plaques. These results were corroborated using postmortem brain samples from AD patients, where microglial HO-1 was found up-regulated in comparison to brain samples from aged matched non-demented patients. This study demonstrates that microglial HO-1 expression increases with aging and especially with AD progression, highlighting HO-1 as a potential biomarker or therapeutic target for AD.
Language	English
Publishing date	2020-07-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9070644
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Article ; Online: Molecular and Pharmacological Modulation of CALHM1 Promote Neuroprotection against Oxygen and Glucose Deprivation in a Model of Hippocampal Slices.

Garrosa, Javier / Paredes, Iñigo / Marambaud, Philippe / López, Manuela G / Cano-Abad, María F

Cells

2020 Volume 9, Issue 3

Abstract: Calcium homeostasis modulator 1 (CALHM1) is a calcium channel involved in the regulation of cytosolic ... ...

Abstract	Calcium homeostasis modulator 1 (CALHM1) is a calcium channel involved in the regulation of cytosolic Ca
MeSH term(s)	Animals ; Brain Ischemia/metabolism ; Calcium/metabolism ; Calcium Channels/drug effects ; Calcium Channels/metabolism ; Cell Death/drug effects ; Cell Survival/drug effects ; Female ; Glucose/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; Male ; Mice, Inbred C57BL ; Neurons/metabolism ; Neuroprotection/drug effects ; Neuroprotective Agents/pharmacology ; Oxygen/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	CALHM1 protein, mouse ; Calcium Channels ; Neuroprotective Agents ; Reactive Oxygen Species ; Glucose (IY9XDZ35W2) ; Oxygen (S88TT14065) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-03-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9030664
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Article ; Online: Adipose tissue as a therapeutic target for vascular damage in Alzheimer's disease.

Bettinetti-Luque, Miriam / Trujillo-Estrada, Laura / Garcia-Fuentes, Eduardo / Andreo-Lopez, Juana / Sanchez-Varo, Raquel / Garrido-Sánchez, Lourdes / Gómez-Mediavilla, Ángela / López, Manuela G / Garcia-Caballero, Melissa / Gutierrez, Antonia / Baglietto-Vargas, David

British journal of pharmacology

2023 Volume 181, Issue 6, Page(s) 840–878

Abstract: Adipose tissue has recently been recognized as an important endocrine organ that plays a crucial role in energy metabolism and in the immune response in many metabolic tissues. With this regard, emerging evidence indicates that an important crosstalk ... ...

Abstract	Adipose tissue has recently been recognized as an important endocrine organ that plays a crucial role in energy metabolism and in the immune response in many metabolic tissues. With this regard, emerging evidence indicates that an important crosstalk exists between the adipose tissue and the brain. However, the contribution of adipose tissue to the development of age-related diseases, including Alzheimer's disease, remains poorly defined. New studies suggest that the adipose tissue modulates brain function through a range of endogenous biologically active factors known as adipokines, which can cross the blood-brain barrier to reach the target areas in the brain or to regulate the function of the blood-brain barrier. In this review, we discuss the effects of several adipokines on the physiology of the blood-brain barrier, their contribution to the development of Alzheimer's disease and their therapeutic potential. LINKED ARTICLES: This article is part of a themed issue From Alzheimer's Disease to Vascular Dementia: Different Roads Leading to Cognitive Decline. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Adipokines ; Brain/metabolism ; Adipose Tissue/physiology ; Blood-Brain Barrier/metabolism
Chemical Substances	Adipokines
Language	English
Publishing date	2023-10-03
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.16243
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Article ; Online: Un-biased housekeeping gene panel selection for high-validity gene expression analysis.

Casas, Ana I / Hassan, Ahmed A / Manz, Quirin / Wiwie, Christian / Kleikers, Pamela / Egea, Javier / López, Manuela G / List, Markus / Baumbach, Jan / Schmidt, Harald H H W

Scientific reports

2022 Volume 12, Issue 1, Page(s) 12324

Abstract: Differential gene expression normalised to a single housekeeping (HK) is used to identify disease mechanisms and therapeutic targets. HK gene selection is often arbitrary, potentially introducing systematic error and discordant results. Here we examine ... ...

Abstract	Differential gene expression normalised to a single housekeeping (HK) is used to identify disease mechanisms and therapeutic targets. HK gene selection is often arbitrary, potentially introducing systematic error and discordant results. Here we examine these risks in a disease model of brain hypoxia. We first identified the eight most frequently used HK genes through a systematic review. However, we observe that in both ex-vivo and in vivo, their expression levels varied considerably between conditions. When applying these genes to normalise expression levels of the validated stroke target gene, inducible Nox4, we obtained opposing results. As an alternative tool for unbiased HK gene selection, software tools exist but are limited to individual datasets lacking genome-wide search capability and user-friendly interfaces. We, therefore, developed the HouseKeepR algorithm to rapidly analyse multiple gene expression datasets in a disease-specific manner and rank HK gene candidates according to stability in an unbiased manner. Using a panel of de novo top-ranked HK genes for brain hypoxia, but not single genes, Nox4 induction was consistently reproduced. Thus, differential gene expression analysis is best normalised against a HK gene panel selected in an unbiased manner. HouseKeepR is the first user-friendly, bias-free, and broadly applicable tool to automatically propose suitable HK genes in a tissue- and disease-dependent manner.
MeSH term(s)	Algorithms ; Gene Expression ; Gene Expression Profiling ; Genes, Essential ; Humans ; Hypoxia, Brain
Language	English
Publishing date	2022-07-19
Publishing country	England
Document type	Journal Article ; Systematic Review ; 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/s41598-022-15989-8
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Article ; Online: Small Synthetic Hyaluronan Disaccharide BIS014 Mitigates Neuropathic Pain in Mice.

Padín, Juan-Fernando / Maroto, Marcos / Entrena, José Manuel / Egea, Javier / Montell, Eulàlia / Vergés, Josep / López, Manuela G / Cobos, Enrique J / García, Antonio G

The journal of pain

2022 Volume 24, Issue 1, Page(s) 68–83

Abstract: Neuropathic pain (NP) is a challenging condition to treat, as the need for new drugs to treat NP is an unmet goal. We investigated the analgesic potential of a new sulfated disaccharide compound, named BIS014. Oral administration (p.o.) of this compound ... ...

Abstract	Neuropathic pain (NP) is a challenging condition to treat, as the need for new drugs to treat NP is an unmet goal. We investigated the analgesic potential of a new sulfated disaccharide compound, named BIS014. Oral administration (p.o.) of this compound induced ameliorative effects in formalin-induced nociception and capsaicin-induced secondary mechanical hypersensitivity in mice, but also after partial sciatic nerve transection (spared nerve injury), chemotherapy (paclitaxel)-induced NP, and diabetic neuropathy induced by streptozotocin. Importantly, BIS014, at doses active on neuropathic hypersensitivity (60 mg/kg/p.o.), did not alter exploratory activity or motor coordination (in the rotarod test), unlike a standard dose of gabapentin (40 mg/kg/p.o.) which although inducing antiallodynic effects on the NP models, it also markedly decreased exploration and motor coordination. In docking and molecular dynamic simulation studies, BIS014 interacted with TRPV
MeSH term(s)	Mice ; Animals ; Capsaicin/adverse effects ; Hyaluronic Acid/pharmacology ; Gabapentin ; TRPV Cation Channels ; Neuralgia ; Hyperalgesia/drug therapy
Chemical Substances	Capsaicin (S07O44R1ZM) ; Hyaluronic Acid (9004-61-9) ; Gabapentin (6CW7F3G59X) ; TRPV Cation Channels
Language	English
Publishing date	2022-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2018789-0
ISSN	1528-8447 ; 1526-5900
ISSN (online)	1528-8447
ISSN	1526-5900
DOI	10.1016/j.jpain.2022.07.014
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Article ; Online: Protective role of microglial HO-1 blockade in aging: Implication of iron metabolism.

Fernández-Mendívil, Cristina / Luengo, Enrique / Trigo-Alonso, Paula / García-Magro, Nuria / Negredo, Pilar / López, Manuela G

Redox biology

2020 Volume 38, Page(s) 101789

Abstract: Heme oxygenase-1 (HO-1) is an inducible enzyme known for its anti-inflammatory, antioxidant and neuroprotective effects. However, increased expression of HO-1 during aging and age-related neurodegenerative diseases have been associated to neurotoxic ... ...

Abstract	Heme oxygenase-1 (HO-1) is an inducible enzyme known for its anti-inflammatory, antioxidant and neuroprotective effects. However, increased expression of HO-1 during aging and age-related neurodegenerative diseases have been associated to neurotoxic ferric iron deposits. Being microglia responsible for the brain's innate immune response, the aim of this study was to understand the role of microglial HO-1 under inflammatory conditions in aged mice. For this purpose, aged wild type (WT) and LysMCreHmox1
MeSH term(s)	Aging ; Animals ; Anti-Inflammatory Agents ; Heme Oxygenase-1/antagonists & inhibitors ; Heme Oxygenase-1/genetics ; Iron/metabolism ; Lipopolysaccharides ; Membrane Proteins ; Mice ; Microglia
Chemical Substances	Anti-Inflammatory Agents ; Lipopolysaccharides ; Membrane Proteins ; Iron (E1UOL152H7) ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2020-11-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101789
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