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Pharmaceutics
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Drug Targeting for CNS Disease
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Drug Targeting for CNS Disease

A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to the section "Drug Targeting and Design".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 30504

Special Issue Editors

Dr. Dorota Łażewska

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Guest Editor
Chair of Technology and Biotechnology of Medical Remedies, Faculty of Pharmacy, Jagiellonian University Medical College in Kraków, Ul. Medyczna 9, 30-688 Kraków, Poland
Interests: medicinal chemistry; multitarget ligands; drug design; synthesis; neurodegenerative disorders; histamine H3 receptors
Special Issues, Collections and Topics in MDPI journals
Dr. Anna Stasiak

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Guest Editor
Department of Hormone Biochemistry, Faculty of Medicine, Medical University of Lodz, Żeligowskiego 7/9 Str., 90-752 Lodz, Poland
Interests: neurodegeneration; CNS diseases; Alzheimer's disease; Parkinson's disease; novel treatments for CNS diseases; neuroprotective agents; dual targeting drugs; multi-targeting drugs; histamine; histamine receptors; biogenic amines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Central nervous system (CNS) diseases (neurodegenerative, neuropsychiatric) have a chronic and progressive character, cause significant morbidity and mortality, and have become a major medical and socioeconomic problem in recent years. To date, the etiology of CNS diseases has not been fully explained. However, it was confirmed that CNS pathologies are usually connected with complex disturbances which simultaneously affect a few neurotransmission systems, often characterized with a progressive loss of neurons in certain brain areas and relate to some common features/disorders (association with age, partially/fully genetic predisposition, protein misfolding and aggregation in brain tissue, inflammatory response and oxidative neuronal injuries, excitotoxicity, mitochondrial dysfunctions, and morphological features of apoptosis).

Current treatment of CNS diseases is largely symptomatic, and it does not bring satisfactory therapeutic effects. Today, there is a crucial need to design strategies for new drug development based on a better understanding of the biochemical mechanisms underlying the pathological conditions and on molecular targeting of therapeutic molecules based thereupon. Currently, many compounds are being tested out. Experimental and clinical observations reveal that nonselective, multipotent drugs appear to be more effective. According to the most recent trends, we should apply therapeutic tools which will simultaneously affect various systems (dual targeting drugs, multitargeting drugs). Thus, CNS diseases are still a huge challenge for researchers.

In this Special Issue of Pharmaceutics titled “Drug Targeting for CNS Diseases”, we invite researchers from both academia and industry to publish their latest research related to CNS diseases. Original papers and reviews on neurodegenerative diseases (e.g., Alzheimer's, Parkinson’s, Huntington’s diseases), mental diseases (e.g., depression), addictions or cancer as well as molecular targets involved in these diseases are welcome. Covered topics include (but are not limited to) the search for new active compounds (medicines) along with pharmacological and pharmacokinetic evaluation. All preclinical (including in vitro, ex vivo, and in vivo tests) as well as clinical studies for the prevention or treatment of CNS diseases are invited.

We are looking forward for your contribution.

Dr. Dorota Łażewska
Dr. Anna Stasiak
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceutics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • CNS diseases
  • neurodegeneration
  • neuroinflammation
  • novel treatments for CNS diseases/drug development for CNS diseases
  • neuroprotective agents
  • dual targeting drugs
  • multi-targeting drugs
  • therapeutic potential of newly drugs for CNS diseases
  • ADMETox studies
  • in vitro/ex vivo/in vivo tests
  • preclinical studies
  • clinical studies

Related Special Issue

Published Papers (10 papers)

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Research

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16 pages, 2166 KiB  
Article
DNAJB6-Containing Extracellular Vesicles as Chaperone Delivery Systems: A Proteomic Analysis
by Bhagyashree S. Joshi, Hector Garcia Romeu, Aldy Aliyandi, Marcel P. de Vries and Inge S. Zuhorn
Pharmaceutics 2022, 14(11), 2485; https://doi.org/10.3390/pharmaceutics14112485 - 17 Nov 2022
Cited by 1 | Viewed by 1504
Abstract
Cell-derived extracellular vesicles (EVs) are effectors of cell-to-cell communication that are in the spotlight as promising candidates for in vivo drug delivery because of their ability to enter cells and deliver cargo. For example, proteins of interest can be loaded into EVs to [...] Read more.
Cell-derived extracellular vesicles (EVs) are effectors of cell-to-cell communication that are in the spotlight as promising candidates for in vivo drug delivery because of their ability to enter cells and deliver cargo. For example, proteins of interest can be loaded into EVs to mediate protein transfer into target cells. To determine causality between EV content and function, which is also important to assess the clinical safety of EVs, it is crucial to comprehensively characterize their complete molecular composition. Here, we investigated EVs loaded with the chaperone protein DNAJB6. Chaperone proteins assist in protein folding and have been suggested to alleviate protein aggregation diseases, such as Alzheimer’s disease and Huntington’s disease. We analyzed and compared the proteome of EVs isolated from wildtype HEK293T cells with that of EVs from HEK 293T cells overexpressing DNAJB6-WT or loss-of-function mutant DNAJB6-M3. Comprehensive analysis of proteomics data showed enhanced levels of DNAJB6 as well as protein-folding-related proteins in EVs derived from DNAJB6-overexpression cells. Interestingly, upregulation of a chaperone and its protein-folding-related proteins resulted in downregulation of another chaperone plus its related proteins, and vice versa. This implies the presence of compensatory mechanisms in the cellular expression of chaperones. Collectively, we provide the proteomic EV signatures underlying EV mediated DNAJB6 transmission by HEK293T cells, with the aim of establishing a causal relationship between EV protein content and EV function. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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12 pages, 1587 KiB  
Article
Increased Expression and Activity of Brain Cortical cPLA2 Due to Chronic Lipopolysaccharide Administration in Mouse Model of Familial Alzheimer’s Disease
by Mikko Gynther, Mariana Leal Estrada, Sanna Loppi, Paula Korhonen, Katja M. Kanninen, Tarja Malm, Jari Koistinaho, Seppo Auriola, Gert Fricker and Elena Puris
Pharmaceutics 2022, 14(11), 2438; https://doi.org/10.3390/pharmaceutics14112438 - 10 Nov 2022
Cited by 3 | Viewed by 1663
Abstract
Cytosolic phospholipase A2 (cPLA2) is an enzyme regulating membrane phospholipid homeostasis and the release of arachidonic acid utilized in inflammatory responses. It represents an attractive target for the treatment of Alzheimer’s disease (AD). Previously, we showed that lipopolysaccharide (LPS)-induced systemic inflammation caused abnormal [...] Read more.
Cytosolic phospholipase A2 (cPLA2) is an enzyme regulating membrane phospholipid homeostasis and the release of arachidonic acid utilized in inflammatory responses. It represents an attractive target for the treatment of Alzheimer’s disease (AD). Previously, we showed that lipopolysaccharide (LPS)-induced systemic inflammation caused abnormal lipid metabolism in the brain of a transgenic AD mouse model (APdE9), which might be associated with potential changes in cPLA2 activity. Here, we investigated changes in cPLA2 expression and activity, as well as the molecular mechanisms underlying these alterations due to chronic LPS administration in the cerebral cortex of female APdE9 mice as compared to saline- and LPS-treated female wild-type mice and saline-treated APdE9 mice. The study revealed the significant effects of genotype LPS treatment on cortical cPLA2 protein expression and activity in APdE9 mice. LPS treatment resulted in nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) activation in the cortex of APdE9 mice. The gene expressions of inflammation markers Il1b and Tnfa were significantly elevated in the cortex of both APdE9 groups compared to the wild-type groups. The study provides evidence of the elevated expression and activity of cPLA2 in the brain cortex of APdE9 mice after chronic LPS treatment, which could be associated with NFkB activation. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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20 pages, 3845 KiB  
Article
Activation of Somatostatin-Expressing Neurons in the Lateral Septum Improves Stress-Induced Depressive-like Behaviors in Mice
by Huanhuan Li, Hyun Hailey Sung and Chunyue Geoffrey Lau
Pharmaceutics 2022, 14(10), 2253; https://doi.org/10.3390/pharmaceutics14102253 - 21 Oct 2022
Cited by 7 | Viewed by 3550
Abstract
Depression is a debilitating mood disorder with highly heterogeneous pathogenesis. The limbic system is well-linked to depression. As an important node in the limbic system, the lateral septum (LS) can modulate multiple affective and motivational behaviors. However, the role of LS in depression [...] Read more.
Depression is a debilitating mood disorder with highly heterogeneous pathogenesis. The limbic system is well-linked to depression. As an important node in the limbic system, the lateral septum (LS) can modulate multiple affective and motivational behaviors. However, the role of LS in depression remains unclear. By using c-Fos expression mapping, we first screened and showed activation of the LS in various depression-related behavioral tests, including the forced swim test (FST), tail suspension test (TST), and sucrose preference test. In the LS, more than 10% of the activated neurons were somatostatin-expressing (SST) neurons. We next developed a microendoscopic calcium imaging method in freely moving mice and revealed that LSSST neural activity increased during mobility in the TST but not open field test. We hypothesize that LSSST neuronal activity is linked to stress and depression. In two mouse models of depression, repeated lipopolysaccharide (LPS) injection and chronic restraint stress (CRS), we showed that LS neuronal activation was suppressed. To examine whether the re-activation of LSSST neurons can be therapeutically beneficial, we optogenetically activated LSSST neurons and produced antidepressant-like effects in LPS-injected mice by increasing TST motility. Moreover, chemogenetic activation of LSSST neurons increased FST struggling in the CRS-exposed mice. Together, these results provide the first evidence of a role for LSSST neurons in regulating depressive-like behaviors in mice and identify them as a potential therapeutic target for neuromodulation-based intervention in depression. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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30 pages, 7042 KiB  
Article
Dual Targeting Ligands—Histamine H3 Receptor Ligands with Monoamine Oxidase B Inhibitory Activity—In Vitro and In Vivo Evaluation
by Dorota Łażewska, Agata Siwek, Agnieszka Olejarz-Maciej, Agata Doroz-Płonka, Anna Wiktorowska-Owczarek, Marta Jóźwiak-Bębenista, David Reiner-Link, Annika Frank, Wioletta Sromek-Trzaskowska, Ewelina Honkisz-Orzechowska, Ewelina Królicka, Holger Stark, Marek Wieczorek, Waldemar Wagner, Katarzyna Kieć-Kononowicz and Anna Stasiak
Pharmaceutics 2022, 14(10), 2187; https://doi.org/10.3390/pharmaceutics14102187 - 13 Oct 2022
Viewed by 1678
Abstract
The clinical symptoms of Parkinson’s disease (PD) appear when dopamine (DA) concentrations in the striatum drops to around 20%. Simultaneous inhibitory effects on histamine H3 receptor (H3R) and MAO B can increase DA levels in the brain. A series of [...] Read more.
The clinical symptoms of Parkinson’s disease (PD) appear when dopamine (DA) concentrations in the striatum drops to around 20%. Simultaneous inhibitory effects on histamine H3 receptor (H3R) and MAO B can increase DA levels in the brain. A series of compounds was designed and tested in vitro for human H3R (hH3R) affinity and inhibitory activity to human MAO B (hMAO B). Results showed different activity of the compounds towards the two biological targets. Most compounds had poor affinity for hH3R (Ki > 500 nM), but very good inhibitory potency for hMAO B (IC50 < 50 nM). After further in vitro testing (modality of MAO B inhibition, permeability in PAMPA assay, cytotoxicity on human astrocyte cell lines), the most promising dual-acting ligand, 1-(3-(4-(tert-butyl)phenoxy)propyl)-2-methylpyrrolidine (13: hH3R: Ki = 25 nM; hMAO B IC50 = 4 nM) was selected for in vivo evaluation. Studies in rats of compound 13, in a dose of 3 mg/kg of body mass, confirmed its antagonistic effects for H3R (decline in food and a water consumption), decline in MAO B activity (>90%) in rat cerebral cortex (CTX), and an increase in DA content in CTX and striatum. Moreover, compound 13 caused a slight increase in noradrenaline, but a reduction in serotonin concentration in CTX. Thus, compound 13 is a promising dual-active ligand for the potential treatment of PD although further studies are needed to confirm this. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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17 pages, 1933 KiB  
Article
The Importance of Endoplasmic Reticulum Stress as a Novel Antidepressant Drug Target and Its Potential Impact on CNS Disorders
by Marta Jóźwiak-Bębenista, Paulina Sokołowska, Małgorzata Siatkowska, Cecilia Analia Panek, Piotr Komorowski, Edward Kowalczyk and Anna Wiktorowska-Owczarek
Pharmaceutics 2022, 14(4), 846; https://doi.org/10.3390/pharmaceutics14040846 - 12 Apr 2022
Cited by 10 | Viewed by 1966
Abstract
Many central nervous system (CNS) diseases, including major depressive disorder (MDD), are underpinned by the unfolded protein response (UPR) activated under endoplasmic reticulum (ER) stress. New, more efficient, therapeutic options for MDD are needed to avoid adverse effects and drug resistance. Therefore, the [...] Read more.
Many central nervous system (CNS) diseases, including major depressive disorder (MDD), are underpinned by the unfolded protein response (UPR) activated under endoplasmic reticulum (ER) stress. New, more efficient, therapeutic options for MDD are needed to avoid adverse effects and drug resistance. Therefore, the aim of the work was to determine whether UPR signalling pathway activation in astrocytes may serve as a novel target for antidepressant drugs. Among the tested antidepressants (escitalopram, amitriptyline, S-ketamine and R-ketamine), only S-ketamine, and to a lesser extent R-ketamine, induced the expression of most ER stress-responsive genes in astrocytes. Furthermore, cell viability and apoptosis measuring assays showed that (R-)S-ketamine did not affect cell survival under ER stress. Under normal conditions, S-ketamine played the key role in increasing the release of brain-derived neurotrophic factor (BDNF), indicating that the drug has a complex mechanism of action in astrocytes, which may contribute to its therapeutic effects. Our findings are the first to shed light on the relationship between old astrocyte specifically induced substance (OASIS) stabilized by ER stress and (R-)S-ketamine; however, the possible involvement of OASIS in the mechanism of therapeutic ketamine action requires further study. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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Review

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18 pages, 3167 KiB  
Review
Cannabinoids and Multiple Sclerosis: A Critical Analysis of Therapeutic Potentials and Safety Concerns
by Roua A. Nouh, Ahmed Kamal and Anwar Abdelnaser
Pharmaceutics 2023, 15(4), 1151; https://doi.org/10.3390/pharmaceutics15041151 - 05 Apr 2023
Cited by 2 | Viewed by 2918
Abstract
Multiple sclerosis (MS) is a complicated condition in which the immune system attacks myelinated axons in the central nervous system (CNS), destroying both myelin and axons to varying degrees. Several environmental, genetic, and epigenetic factors influence the risk of developing the disease and [...] Read more.
Multiple sclerosis (MS) is a complicated condition in which the immune system attacks myelinated axons in the central nervous system (CNS), destroying both myelin and axons to varying degrees. Several environmental, genetic, and epigenetic factors influence the risk of developing the disease and how well it responds to treatment. Cannabinoids have recently sparked renewed interest in their therapeutic applications, with growing evidence for their role in symptom control in MS. Cannabinoids exert their roles through the endogenous cannabinoid (ECB) system, with some reports shedding light on the molecular biology of this system and lending credence to some anecdotal medical claims. The double nature of cannabinoids, which cause both positive and negative effects, comes from their actions on the same receptor. Several mechanisms have been adopted to evade this effect. However, there are still numerous limitations to using cannabinoids to treat MS patients. In this review, we will explore and discuss the molecular effect of cannabinoids on the ECB system, the various factors that affect the response to cannabinoids in the body, including the role of gene polymorphism and its relation to dosage, assessing the positive over the adverse effects of cannabinoids in MS, and finally, exploring the possible functional mechanism of cannabinoids in MS and the current and future progress of cannabinoid therapeutics. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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25 pages, 612 KiB  
Review
Therapeutic Potential of Natural Compounds in Neurodegenerative Diseases: Insights from Clinical Trials
by Stéphanie Andrade, Débora Nunes, Meghna Dabur, Maria J. Ramalho, Maria C. Pereira and Joana A. Loureiro
Pharmaceutics 2023, 15(1), 212; https://doi.org/10.3390/pharmaceutics15010212 - 07 Jan 2023
Cited by 9 | Viewed by 2716
Abstract
Neurodegenerative diseases are caused by the gradual loss of neurons’ function. These neurological illnesses remain incurable, and current medicines only alleviate the symptoms. Given the social and economic burden caused by the rising frequency of neurodegenerative diseases, there is an urgent need for [...] Read more.
Neurodegenerative diseases are caused by the gradual loss of neurons’ function. These neurological illnesses remain incurable, and current medicines only alleviate the symptoms. Given the social and economic burden caused by the rising frequency of neurodegenerative diseases, there is an urgent need for the development of appropriate therapeutics. Natural compounds are gaining popularity as alternatives to synthetic drugs due to their neuroprotective properties and higher biocompatibility. While natural compounds’ therapeutic effects for neurodegenerative disease treatment have been investigated in numerous in vitro and in vivo studies, only few have moved to clinical trials. This article provides the first systematic review of the clinical trials evaluating natural compounds’ safety and efficacy for the treatment of the five most prevalent neurodegenerative disorders: Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington’s disease. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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31 pages, 2667 KiB  
Review
Drug Delivery Systems as a Strategy to Improve the Efficacy of FDA-Approved Alzheimer’s Drugs
by Débora Nunes, Joana A. Loureiro and Maria Carmo Pereira
Pharmaceutics 2022, 14(11), 2296; https://doi.org/10.3390/pharmaceutics14112296 - 26 Oct 2022
Cited by 12 | Viewed by 4140
Abstract
Alzheimer’s disease (AD) is the most common form of dementia, with a high impact worldwide, accounting for more than 46 million cases. The continuous increase of AD demands the fast development of preventive and curative therapeutic strategies that are truly effective. The drugs [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia, with a high impact worldwide, accounting for more than 46 million cases. The continuous increase of AD demands the fast development of preventive and curative therapeutic strategies that are truly effective. The drugs approved for AD treatment are classified into acetylcholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists. The therapeutic effectiveness of those drugs is hindered by their restricted access to the brain due to the blood–brain barrier, low bioavailability, and poor pharmacokinetic properties. In addition, the drugs are reported to have undesirable side effects. Several drug delivery systems (DDSs) have been widely exploited to address these issues. DDSs serve as drug carriers, combining the ability to deliver drugs locally and in a targeted manner with the ability to release them in a controlled and sustained manner. As a result, the pharmacological therapeutic effectiveness is raised, while the unwanted side effects induced by the unspecific distribution decrease. This article reviews the recently developed DDSs to increase the efficacy of Food and Drug Administration-approved AD drugs. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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20 pages, 1765 KiB  
Review
Therapeutic Approach to Alzheimer’s Disease: Current Treatments and New Perspectives
by Teresa Pardo-Moreno, Anabel González-Acedo, Antonio Rivas-Domínguez, Victoria García-Morales, Francisco Jose García-Cozar, Juan Jose Ramos-Rodríguez and Lucía Melguizo-Rodríguez
Pharmaceutics 2022, 14(6), 1117; https://doi.org/10.3390/pharmaceutics14061117 - 24 May 2022
Cited by 67 | Viewed by 7235
Abstract
Alzheimer’s disease (AD) is the most common cause of dementia. The pathophysiology of this disease is characterized by the accumulation of amyloid-β, leading to the formation of senile plaques, and by the intracellular presence of neurofibrillary tangles based on hyperphosphorylated tau protein. In [...] Read more.
Alzheimer’s disease (AD) is the most common cause of dementia. The pathophysiology of this disease is characterized by the accumulation of amyloid-β, leading to the formation of senile plaques, and by the intracellular presence of neurofibrillary tangles based on hyperphosphorylated tau protein. In the therapeutic approach to AD, we can identify three important fronts: the approved drugs currently available for the treatment of the disease, which include aducanumab, donepezil, galantamine, rivastigmine, memantine, and a combination of memantine and donepezil; therapies under investigation that work mainly on Aβ pathology and tau pathology, and which include γ-secretase inhibitors, β-secretase inhibitors, α-secretase modulators, aggregation inhibitors, metal interfering drugs, drugs that enhance Aβ clearance, inhibitors of tau protein hyperphosphorylation, tau protein aggregation inhibitors, and drugs that promote the clearance of tau, and finally, other alternative therapies designed to improve lifestyle, thus contributing to the prevention of the disease. Therefore, the aim of this review was to analyze and describe current treatments and possible future alternatives in the therapeutic approach to AD. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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Other

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17 pages, 584 KiB  
Systematic Review
Angiotensin II Receptor Blockers in the Management of Hypertension in Preventing Cognitive Impairment and Dementia—A Systematic Review
by Elvira D’Silva, Nur Farah Meor Azlan and Jinwei Zhang
Pharmaceutics 2022, 14(10), 2123; https://doi.org/10.3390/pharmaceutics14102123 - 06 Oct 2022
Cited by 3 | Viewed by 1895
Abstract
Hypertension is a known risk factor for cognition-related pathologies including dementia. The National Institute of Health and Care Excellence (NICE) guidelines recommend angiotensin (Ang) II receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) as a first-line treatment for hypertension. Although both ARBs and [...] Read more.
Hypertension is a known risk factor for cognition-related pathologies including dementia. The National Institute of Health and Care Excellence (NICE) guidelines recommend angiotensin (Ang) II receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) as a first-line treatment for hypertension. Although both ARBs and ACEIs show neuroprotective effects, ACEIs show contradictory side effects; therefore, ARBs may be a more viable option. However, trials assessing the effects of ARBs on cognition are scarce and conflicting. Therefore, the aim of this review is to conduct a systematic review and synthesise data on the influence of ARBs on cognition and dementia prevention. Five databases were searched from 1992–2022 to produce 13 randomised controlled trials (RCTs) involving 26,907 patients that compared associations of ARBs against placebos or other antihypertensives on cognition or probable dementia with a minimum duration of 3 months. ARBs showed greater cognitive benefits when compared to hydrochlorothiazide (HCTZ), beta blockers (BB), and ACEIs. Our findings showed that although ARBs are superior to some antihypertensives such as ACEIs, thiazide and beta blockers, they made no difference in comparison to the placebo in all but one sample of patients. The positive effects on cognitive performances are equal to calcium channel blockers (CCBs) and lower than statin. The neuroprotective effects of ARBs are also more beneficial when ARBs are taken at the same time as a statin. Due to these inconsistencies, robust conclusions cannot be made. Future trials are warranted and, if successful, could have positive economic implications and consequently improve quality of life. Full article
(This article belongs to the Special Issue Drug Targeting for CNS Disease)
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