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Review

α1A-Adrenergic Receptor as a Target for Neurocognition: Cautionary Tale from Nicergoline and Quinazoline Non-Selective Blockers

by
Dianne M. Perez
Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
Pharmaceuticals 2025, 18(10), 1425; https://doi.org/10.3390/ph18101425
Submission received: 6 August 2025 / Revised: 3 September 2025 / Accepted: 18 September 2025 / Published: 23 September 2025
(This article belongs to the Special Issue Pharmacotherapy for Alzheimer’s Disease)
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Abstract

Decades ago, previous studies that used non-selective ergot derivatives suggested that blockage of the α1A-adrenergic receptor mildly increased cognition through increased blood flow to the brain due to vasodilation and, thus, could be used as a treatment for dementia. However, further studies indicated that nicergoline was non-specific and hit many different targets. Today, a similar scenario is developing with the use of non-selective α1-AR antagonists of the quinazoline class, referred to as “osins”, as potential treatments for COVID-19/SARS, post-traumatic stress disorder, cancer, and neurodegenerative disorders, such as Parkinson’s, Alzheimer’s, and amyotrophic lateral sclerosis. While there is extensive evidence of neuroprotection from many clinical trials, the mechanism of action of quinazolines is often not α1-AR-mediated but keyed to its glycolysis-enhancing effects through activation of the enzyme phosphoglycerate kinase 1 (PGK1). These studies have incorrectly labeled the α1A-adrenergic receptor as an “old target” to treat Alzheimer’s and other neurocognitive diseases, hampering drug development. This review will summarize these and other studies to indicate that activation, not blockage, of norepinephrine’s actions, through α1A-AR, mediates cognitive, memory, and neuroprotective functions that may reverse the progression of neurocognitive diseases.

1. Introduction

Norepinephrine and the Adrenergic Receptors: Each Subtype Can Have Distinct Functions

Adrenergic Receptors (ARs) are G-Protein Coupled Receptors (GPCRs) that regulate neurotransmission and the sympathetic nervous system through different ARs that bind the neurotransmitter, norepinephrine (NE), and the neurohormone, epinephrine (EPI). Drugs that target GPCRs represent about 30% of all current clinical drugs because of the receptor’s cell surface localization and well-characterized pharmacological and physiological hormonal functions. There is a total of nine AR family members (β1, β2, β3, α2A, α2B, α2C, α1A, α1B, and α1D) that bind NE/EPI, but they can regulate distinct functions through coupling to different G-proteins and signaling pathways. Many of the distinct functions of each subclass of ARs are driven by tissue localization, relative density, and signal transduction differences.
β-ARs couple mainly through Gs, a GTP-binding protein (G-protein) that stimulates adenylate cyclase, to produce cyclic adenosine 3′, 5′,-monophosphate (cAMP), which then activates the protein kinase A (PKA) signaling pathway. Because it was the first GPCR that was cloned, subtype-distinct functions are more defined, facilitating drug development. β1-ARs are highly expressed in the heart. β-blockers are used to slow down the heart rate and reduce cardiac workload to treat heart failure. β2-ARs are highly expressed in the lungs. β2-ARs agonists are used to treat asthma by dilating the smooth muscle of the bronchioles to increase air flow to the lungs. β3-AR agonists are being explored to regulate metabolic disorders and overactive bladder [1].
α2-ARs couple mainly through Gi, a GTP-binding protein that inhibits adenylate cyclase, which decreases the production of cAMP, and are often used to regulate the cAMP levels induced through β-ARs. A well-known regulation of this type is insulin secretion. α2A- and α2C-ARs are known to regulate neurotransmission by their location on synaptic terminals. Actions of α2A/C-AR inhibit the release of NE, which is referred to as an auto-receptor, but do so at different sympathetic stimulation frequencies [2]. α2A-AR activation also leads to a decrease in blood pressure, while α2B-AR stimulation may counteract this effect by causing direct vasoconstriction. α2C-ARs participate in vasoconstriction after exposure to cold temperature [3]. Clinically, several types of non-selective α2-AR agonists, such as clonidine, medetomidine, and brimonidine, are being used to treat patients for sedation or for a variety of symptoms, such as hypertension, glaucoma, tumor pain, postoperative pain, shivering, or to block the symptoms of sympathetic overactivity, but all produce unwanted side effects.
α1-ARs were the last of the ARs to be cloned and characterized. α1-ARs canonically couple to Gq, a GTP-binding protein that activates phospholipase C (PLC), which causes the hydrolysis of membrane-bound phosphatidylinositol 4,5-bisphosphate to release inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 binds to receptors located on the endoplasmic reticulum, causing the release of calcium that constricts the smooth muscle in blood vessels, increasing blood pressure. DAG activates protein kinase C (PKC), an enzymatic effector that phosphorylates many proteins to amplify signals downstream in the signaling cascade. The non-selective α1-AR antagonists, prazosin, terazosin, doxazosin, tamsulosin, and alfuzosin are approved to treat the symptoms of benign prostatic hyperplasia by relaxing prostatic smooth muscle to improve urinary flow. They are taken at night to minimize effects on blood pressure. Because the receptor target invokes unwanted side effects on blood pressure, subtype-specific drug development for the clinic has not been a high priority. However, transgenic and knockout (KO) mouse models have identified some key subtype-selective functions that may be targeted for subtype-selective drug development. It is now recognized that α1A-AR activation is cardioprotective in heart failure and ischemia, while α1B-AR overactivity is cardiac maladaptive [4]. As detailed later, α1A-AR activation has also been shown to be cognitive and memory enhancing, while α1B-AR activation is pro-epileptic and neurodegenerative [5]. α1-ARs, as with all GPCRs, can signal directly through their main signaling cascade or through crosstalk to increase signal diversity via G protein-dependent and independent pathways, spatio-temporal mechanisms, and biased agonistic signaling [6,7,8,9].
There is evidence that each AR family and subtype can regulate distinct functions and physiology and has the potential to be therapeutically targeted to alleviate disease symptoms. However, there is a distinct lack of sufficiently selective activators or blockers that has hampered these assessments, and the use of non-selective agents leads to many unwanted side effects and may have additional off-targets; such is the case for nicergoline and the non-selective quinazoline α1-AR antagonists.
This review will summarize the pharmacological and therapeutic functions of nicergoline and the non-selective quinazoline α1-AR antagonists, prazosin, doxazosin, terazosin, and alfuzosin (Figure 1) as they pertain to neuroprotection and remediation of the symptoms of dementia or Alzheimer’s disease. Decades of research have supported the hypothesis that activation, not blockage, of NE function through its many subtypes of ARs is pro-cognitive and may be of therapeutic benefit in Alzheimer’s disease. In the case of nicergoline, this review will highlight the numerous physiological functions and complex mechanism of action mediated through targeting several neurotransmitters, not just α1-AR. In the case of non-selective quinazoline α1-AR antagonists, which are prescribed to treat benign prostatic hyperplasia (BPH) through the relaxation of smooth muscle, this review will highlight their ability to activate PGK1, a non-α1-AR-mediated mechanism, to increase glycolysis to remediate neurodegenerative diseases. Studies that explore the cognitive ability of tamsulosin, an α1-AR antagonist also used to treat BPH, but does not contain the quinazoline pharmacophore and is somewhat selective for the α1A-AR subtype, have shown that it does not bind and activate PGK1 and displays opposite cognitive functions compared to quinazoline α1-AR antagonists. Thus, this supports the interpretation that quinazoline α1-AR antagonists’ effects, as they pertain to neurodegeneration and Alzheimer’s disease, are non-α1-AR-mediated and “off-target”. In both scenarios of blocking α1-ARs by either nicergoline or quinazoline α1-AR antagonists, the interpretation that inhibiting α1-AR activation would be of therapeutic benefit in dementia or Alzheimer’s disease is flawed.

2. NE and AR Activation Increase Memory and Cognition

There is an abundance of evidence that NE activation enhances learning, memory, and neuroprotective signals [10,11]. Cognitive enhancement can be achieved through direct stimulation of the ARs or through the use of selective NE reuptake inhibitors to increase NE levels in the frontal cortex or hippocampus [12]. NE is the main neurotransmitter synthesized by locus coeruleus neurons that degenerate and is an early pathology in Alzheimer’s disease [13]. Mice unable to synthesize NE by genetic deletion of the dopamine β-hydroxylase gene show cognitive dysfunction, synaptic, and long-term potentiation (LTP) deficits [14,15]. Specific areas of learning and memory affected by NE include focused and flexible attention, increased arousal and alertness, working memory, and memory formation and retrieval [5]. Using KO and overexpressed mouse models, in addition to various clinical studies, the activation of all AR subtypes (β, α2, α1) indicated some level of enhanced cognitive function [16,17,18]. Of note, meta-analysis of clinical trials where NE was stimulated with various agonists of the AR family has established a beneficial effect on cognition [19]. The memory/cognitive-inducing signals of NE primarily involve cyclic adenosine monophosphate (cAMP) production, phosphorylation of cyclic AMP response element-binding protein (CREB), or Exchange Proteins Activated by cAMP (EPAC) [20,21,22], which α1-ARs and β-AR canonical pathways can also regulate [23,24,25,26]. In addition, Extracellular Signal-Regulated Kinase (ERK) is also an NE-mediated cognitive and neuroprotective signal [20,27,28], also mediating the transcription and translation of proteins that increase metaplasticity [29].

3. α1-AR Activation Increases Cognition and Memory

α1-AR activation, particularly the α1A-AR subtype, has significant roles in the regulation of synaptic efficacy, both short- and long-term synaptic plasticity, and different types of memory [5]. Most brain areas affected in Alzheimer’s disease express α1-AR, and they mediate various functions of learning and memory. α1-ARs increased LTP and LTD (long-term depression) in the prefrontal cortex, neocortex, ventral tegmental area, and hippocampus, and are associated with increased cognition. Both LTP and LTD may impart different forms of synaptic information during spatial learning. α1-AR activation can enhance memory recall, retention, and consolidation in the entorhinal cortex, fear-conditioned memory in the amygdala, and spatial memory and associative learning in the prefrontal cortex and hippocampus [5].
The generation of transgenic mouse models of the α1-AR subtypes and the development of highly selective subtype-selective ligands that can discriminate the subtypes have supported the hypothesis that activation of NE through α1A-AR generates a pro-cognitive and neuroprotective profile through regulation of neurogenesis and both short-term and long-term synaptic plasticity [5]. While all three of the α1-AR subtypes are associated with various aspects of learning and memory, α1A-AR shows the most promise as a therapeutic in AD. α1A-AR protein and RNA levels are downregulated in AD and in an AD mouse model [30,31], and polymorphisms are linked with AD [32] and schizophrenia [33]. In addition, a positive allosteric modulator of α1A-AR was shown in pre-clinical studies to improve long-term synaptic plasticity and cognition, and clear β-amyloids in AD mouse models better than donepezil (i.e., Aricept) [34].

4. Nicergoline, an Ergot Derivative Originally Proposed to Treat Dementia Through Vasodilation, Does Not Specifically Block α1A-AR

While there is substantial evidence supporting the activation of α1A-AR as a therapeutic route to treat AD, some previous studies have suggested that blocking α1-AR through nicergoline would result in a pro-cognitive profile due to an increased blood flow to the brain. As reviewed below, while nicergoline has a pro-cognitive profile, it is not mediated through α1A-ARs; however, through the years, this outdated understanding of nicergoline has muddled the field of α1-AR-based therapeutic development.
Nicergoline (Figure 1), chemically defined as 8-beta-(5-bromonicotinoylhydroxymethyl)-1,6-dimethyl-10alpha-metoxyergoline, is a bioactive, alkaloid molecule derived from ergot fungus that was first described more than five decades ago as a neuroprotective agent to treat dementia-related conditions in the elderly. Nicergoline is known under various trade names such as Sermion and Adavin, but is not FDA-approved. In fact, nicergoline was banned in Europe in 2013 along with other ergot derivatives because of its side effects. However, its noted efficacy in clinical trials to improve cognition, but incorrect initial assessment on selective α1A-AR antagonism has led to the speculation that blocking, not activating this receptor, would be therapeutic for neurocognitive diseases.
Most neurological studies using nicergoline focused on cerebrovascular disorders, and there is only limited data for AD. Since 1972, hundreds of clinical trials using nicergoline have been performed with various criteria and endpoint evaluations. In 2001, a meta-analysis of 11 of these clinical trials was performed that included only studies that were double-blinded and placebo-controlled and assessed mostly older patients with cognitive impairment from a wide variety of clinical origins. The results of this meta-analysis provided evidence that nicergoline can improve cognition but also indicated some problems with the tolerance of this medication [35]. Since then, more recent clinical studies have confirmed that nicergoline enhances the cognitive performance of patients with dementia [36]. Nicergoline also confers neuroprotective benefits, which aid in potentially lessening age-related cognitive decline [37,38]. However, the drug has never been compared to other therapies, such as donepezil, that treat cognitive disorders as a benchmark. Paradoxically, a recent meta-analysis of 31,881 dementia-related reported adverse events has identified that nicergoline has a high risk of inducing the dementia it was thought to protect against [39].
Cognitive benefits of nicergoline may be through increased vasodilation, resulting in increased cerebral and peripheral blood flow, improving the symptoms of vascular dementia and neurodegeneration, but the effects are complex due to simultaneously blocking α1-ARs, centrally acting α2-ARs, and other neurotransmitter receptors [40]. In fact, various studies (dog, cat, rabbit, rat, mouse, and guinea pig) showed that nicergoline affects blood pressure and heart rate only slightly and increases the blood flow in the brain and hind limb without affecting the splanchnic and aortic flow in normal animals, indicating that not only α1-ARs are being blocked [41,42]. Nicergoline has numerous pharmacological and physiological effects in addition to vasodilation, such as increased cholinergic and catecholaminergic activity, increased metabolism, antioxidant and neurotrophic effects, and anti-platelet aggregation, most likely due to its affinity for many different receptor systems [43]. Cognitive benefits can also be due to increased acetylcholine release [44] and enhancement of choline acetyltransferase activity [45], which correlated with improvement in rodent memory tests [46]. In addition, nicergoline is neurotrophic, increases nerve growth factor in aged rats [47], and induces antioxidant effects [48,49] that may protect against the loss of cholinergic neurons.
The very broad spectrum of nicergoline’s functions is consistent with its non-selective nature. Originally described as a vasodilating α1-AR blocker [50] and later as an α1A-AR selective antagonist (pA2 = 8.8 or 3 nM) [51], this classification was solely based upon its sensitivity to the alkylating agent, chloroethylclonidine (CEC), which has been shown to be non-selective [52,53] and not useful in discriminating between the α1-AR subtypes. In addition to blocking α1-AR non-selectively, nicergoline has similar affinity in blocking several serotonin receptors (IC50 = 6 nM) and shows moderate affinity for dopamine, α2-ARs, and muscarinic acetylcholine M1 and M2 receptors [37,38]. Unfortunately, most of these studies used tissue preparations and were not pharmacologically characterized in any cloned and isolated receptor systems, which were available and are considered a gold standard to characterize a ligand’s selectivity. The IC50 of nicergoline in vitro has been reported to be 0.2 nM [54], about 10-fold higher affinity than any tested receptor, suggesting there may be additional unknown targets. Considering the non-selective nature of nicergoline, the previous hypothesis that cognition increases due to blocking α1A-AR activity does not seem likely.

5. Non-Selective Quinazoline-Derived α1-AR Blockers—The “Osins” Cause “Off-Target” Neuroprotective Effects

While nicergoline does not share any obvious structural features with common α1-AR blockers (Figure 1), the broad neuroprotective effects of the non-selective α1-AR antagonists, prazosin, doxazosin, and terazosin (often referred to as the “osins”) are well-documented [54,55,56,57,58,59,60,61,62,63]. These drugs are approved and considered a first-line treatment for BPH by the relaxation of prostatic and bladder smooth muscle, a basic α1-AR physiological function [64]. However, neuroprotective effects are not α1-AR-mediated but through the binding and activation of phosphoglycerate kinase (PGK1)-mediated ATP production. PGK1 is the first enzyme in the glycolysis pathway and converts ADP into ATP, which can fuel the high-energy requirements of the brain. Terazosin increases the release of ATP by competing for the same binding site as ADP in PGK1, thereby exerting an agonistic effect [65]. However, at high concentrations, it can inhibit PGK1 activity [66].
Neuroprotection may be mediated through metabolism-based therapies. In a degenerating motor neuron-based model of amyotrophic lateral sclerosis, increased glucose uptake and metabolism are neuroprotective [67]. As heart failure is considered an energy-starved disease [68], so are several neurodegenerative diseases. The brain utilizes glucose as its primary fuel for its high energy demands, accounting for 20% of whole-body energy consumption, but comprises only 2% of body mass [69,70]. In congruence, bioenergetic and mitochondrial dysfunction are commonly seen in neurodegenerative diseases and can modulate onset and progression [67,71,72]. It is hypothesized that increased PGK1-mediated ATP availability in neurons allows better adaptation to the cellular challenges of aging and protein aggregation, supported by epidemiologic cohort studies of the “osins” in the treatment of Parkinson’s disease [73,74] and among patients using “osins” for benign prostatic hyperplasia (BPH) [75].
While the neuroprotective benefits of quinazoline-based α1-AR antagonists are substantially evidenced, there is conflicting evidence on their role in mediating cognition as a primary outcome. A clinical trial in AD patients concluded that prazosin was effective in relieving agitation and aggression, but cognition was not assessed [76]. A meta-analysis of seven independent clinical studies found no clear association between non-selective α1-AR antagonists and modulation of cognition, with varied results indicating increased, decreased, or no change in the risk of developing dementia [77]. However, all of the neuroprotection and/or cognitive studies utilized these non-selective antagonists for the α1-AR subtypes and not any other α1-AR antagonists that are more subtype-selective, such as 5-methylurapidil. In general, any agent that reduces blood pressure can have indirect effects on cognition in the elderly and delay the risk of developing dementia [78], but there is a lack of direct evidence that non-selective quinazoline antagonists of α1-ARs can alter cognition and whether it is through PGK1 or α1-AR activity.
Quinazolines are an interesting chemical moiety and have garnered considerable interest in drug development. It was originally discovered in febrifugine, a quinazoline alkaloid with antimalarial potential [79]. Pharmacologically active molecules based on quinazoline scaffolds are strong chemotherapeutic drugs with anticancer, antimicrobial, antioxidant, anti-inflammatory, and antidiabetic properties [80]. As discussed previously, quinazolines also activate PGK1. Interestingly, quinazolines share their pharmacophore with that of acetylcholinesterase inhibitors (AChEIs), which are used as a current treatment for Alzheimer’s disease. A field-based 3D-QSAR (Quantitative Structure–Activity Relationship) pharmacophore design model of quinazoline-based AChEIs identified three novel lead molecules as potent AChEIs [81]. Quinazoline can also inhibit monoamine oxidases (MAO); the MAO-A subtype metabolizes NE, epinephrine, and serotonin. An inhibitor would increase the levels of these neurotransmitters and is also used to treat Alzheimer’s disease and Parkinson’s [82]. As Alzheimer’s disease is complex and involves multiple pathways, a drug possessing a single target mechanism may not be effective enough. Quinazolines hold promise in this regard.

6. Tamsulosin Is Not a Quinazoline and May Increase Risk for Dementia

PKG1 binding and activation have also been demonstrated in other related quinazoline-related α1-AR antagonists such as alfuzosin, prazosin, and doxazosin (Figure 1) [65], but not tamsulosin, an α1-AR blocker with some selectivity (10-fold) for α1A/D-AR [83,84]. Tamsulosin does not contain the quinazoline motif and does not interact with PGK1 [55], supporting that quinazoline α1-AR antagonists have “off-target” effects. Tamsulosin shares some structural motifs with another somewhat selective non-quinazoline α1A-AR antagonist, WB4101 (Figure 1). Tamsulosin also does not appear to mediate anti-inflammatory or neuroprotective effects [63,76], thus confirming that quinazoline’s neuroprotective effects are non-α1-AR-mediated. In further support, a cohort study of individuals treated with terazosin, alfuzosin, or doxazosin for urinary problems indicated a lower risk of developing Parkinson’s disease (PD) when compared to patients treated with tamsulosin [73]. In fact, tamsulosin was suggested to even potentiate PD progression [75], increase the risk of dementia in older men with BPH [85], and impair memory acquisition and consolidation in mice [86], suggesting that blocking α1A-AR impairs cognition. While designed to be α1A-AR selective, tamsulosin has 10-fold selectivity only against the α1B-AR subtype but has equal affinity between α1A- and α1D-AR [83,84]. In contrast to the potential anti-cognitive effects of tamsulosin and recent work indicating that a highly selective α1A-AR positive allosteric activator can reverse AD in pre-clinical studies in two different AD mouse models [34], a recent publication using a neuron-specific intracerebroventricular adeno-associated viral delivery of short-hairpin RNA to knockdown the α1A-AR in a 3xTG AD mouse model indicated reversal of cognitive, neuroinflammatory deficits and taupathology [87]. However, receptor expression levels were not assessed using a radiolabeled binding study, but were assessed using a peptide-generated polyclonal antibody, which was not verified against α1A-AR knockout (KO) tissues. These antibodies have been tested in two independent studies using the KO mouse models as negative controls and indicated that all commercially available antibodies against the α1-AR subtypes are non-specific [88,89]. In addition, confirmatory studies in [87] were performed using terazosin and without reference to or discussion of possible PGK1 activity, the differential role of α1-AR subtypes, or prior genetic studies. KO of the α1-AR subtypes using genetic manipulation and verified through radioligand binding studies have indicated that various aspects of learning and memory are impaired with KO in α1A-AR [16], α1B-AR [90,91], and α1D [92]. Overexpression of the α1-AR subtypes indicates differential roles in the brain, with overexpression of the α1A-AR enhancing synaptic plasticity, cognition [12], and lifespan [93], while overexpression of α1B-AR leads to neurodegeneration [94,95], synucleinopathy [96], shortened life span [95], and seizures [97].

7. Conclusions

Activation of NE-mediated neurotransmission via the AR family (α1, α2, β) is associated with increased cognitive functions, supported by AR knock-out and transgenic mouse models and clinical trials. However, several prominent studies using nicergoline, which is non-selective, in addition to quinazoline antagonists of the α1-AR, which target PGK1 and enhance glycolysis, have suggested that blockage and not activation of the α1-ARs, specifically the α1A-AR subtype, is a suitable therapeutic pathway to treat neurocognitive diseases. While the cognitive and/or neuroprotective benefits of nicergoline and the “osins” are well-evidenced, their effects are likely due to non-α1-AR-mediated activity through “off-target” pathways, and studies using these agents should be interpreted with caution.
In future directions for drug development, while quinazoline α1-AR antagonists’ neuroprotective benefits are not α1-AR-mediated, this does not decrease their importance as a potential therapeutic for Alzheimer’s disease. The quinazoline scaffolds could be modified to increase affinity for PGK1 and decrease affinity for α1-AR, preventing α1-AR inhibition. In the development of α1A-AR agonists, highly specific agonists would need to be designed, which is possible as the structure of a mildly selective A60613 agonist bound with α1A-AR has been published [98]. However, as α1-AR agonists increase blood pressure, a drug would need to be signal-biased against the pathways that regulate blood pressure but still activate the cognitive-enhancing pathways. Such is the case for a positive allosteric modulator of the α1A-AR that was shown in pre-clinical studies to improve long-term synaptic plasticity and cognition, and clear β-amyloids in AD mouse models better than donepezil (i.e., Aricept) but without effects on blood pressure [34]. With the structure of the α1A-AR bound to a mixed allosteric modulator [99], we speculate that the design of additional positive allosteric modulators with greater efficacy and potency may be possible.

Funding

This work was supported by grants from the National Institute of Aging RO1AG066627 and the Alzheimer’s Drug Discovery Foundation (ADDF)-Program to Accelerate Clinical Trials (PACT) to D.M.P.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study.

Conflicts of Interest

The author declares the following competing interests: WO-2020219721, US Patent (US20220227717), European Patent (EP3958851B1). Inventors: PEREZ, Dianne M.; STAUFFER, Shaun R.; MACDONALD, Jonathan. Allosteric Activators of the Alpha1A-Adrenergic receptor.

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Pharmaceuticals 18 01425 g001
Figure 1. Chemical structures of nicergoline, the quinazoline “osins” (terazosin, prazosin, doxazosin, alfuzosin), and the α1A-AR mildly selective non-quinazoline blockers, tamsulosin and WB4101.
Figure 1. Chemical structures of nicergoline, the quinazoline “osins” (terazosin, prazosin, doxazosin, alfuzosin), and the α1A-AR mildly selective non-quinazoline blockers, tamsulosin and WB4101.
Pharmaceuticals 18 01425 g001
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Perez, D.M. α1A-Adrenergic Receptor as a Target for Neurocognition: Cautionary Tale from Nicergoline and Quinazoline Non-Selective Blockers. Pharmaceuticals 2025, 18, 1425. https://doi.org/10.3390/ph18101425

AMA Style

Perez DM. α1A-Adrenergic Receptor as a Target for Neurocognition: Cautionary Tale from Nicergoline and Quinazoline Non-Selective Blockers. Pharmaceuticals. 2025; 18(10):1425. https://doi.org/10.3390/ph18101425

Chicago/Turabian Style

Perez, Dianne M. 2025. "α1A-Adrenergic Receptor as a Target for Neurocognition: Cautionary Tale from Nicergoline and Quinazoline Non-Selective Blockers" Pharmaceuticals 18, no. 10: 1425. https://doi.org/10.3390/ph18101425

APA Style

Perez, D. M. (2025). α1A-Adrenergic Receptor as a Target for Neurocognition: Cautionary Tale from Nicergoline and Quinazoline Non-Selective Blockers. Pharmaceuticals, 18(10), 1425. https://doi.org/10.3390/ph18101425

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