The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform

Abraham Fisher - One of the best experts on this subject based on the ideXlab platform.

  • M1 muscarinic agonists target major hallmarks of Alzheimer's disease--an update.
    Current Alzheimer research, 2007
    Co-Authors: Abraham Fisher
    Abstract:

    UNLABELLED The M1 muscarinic receptor (M1 mAChR), preserved in Alzheimer's disease (AD), is a pivotal target that links major hallmarks of AD, e.g. cholinergic deficiency, cognitive dysfunctions, beta-amyloid (Abeta) and tau pathologies. Some muscarinic agonists, while effective in AD, had limited clinical value due to adverse effects and lack of M1 selectivity. The M1 selective muscarinic agonists AF102B [Cevimeline], AF150(S) and AF267B - i) elevated alphaAPPs, decreased Abeta levels and tau hyperphosphorylation, and blocked Abeta-induced neurotoxicity, in vitro, via M1 mAChR-modulation of kinases (e.g. PKC, MAPK and GSK3beta); ii) restored cognitive deficits, cholinergic markers, and decreased tau hyperphosphorylation in relevant models with a wide safety margin. AF267B decreased brain Abeta levels in hypercholesterolemic rabbits and decreased CSF Abeta42 in rabbits and removed vascular Abeta42 deposition from cortex in cholinotoxin-treated rabbits. In 3x transgenic-AD mice that recapitulate the major pathologies and cognitive deficits of AD, chronic AF267B treatment rescued cognitive deficits and decreased Abeta42 and tau pathologies in the cortex and hippocampus (not amygdala), via M1 mAChR-activation of ADAM17/TACE and decreased BACE1 steady state levels and inhibition of GSK3beta, extending findings from above. CONCLUSIONS A comprehensive therapy should target all AD hallmarks, regardless of the culprit(s) responsible for the disease. In this context, AF267B is the 1(st) reported low MW CNS-penetrable mono-therapy that meets this challenge. Clinical trials will determine if AF267B may become an important therapy in AD.

  • m1 muscarinic agonists can modulate some of the hallmarks in alzheimer s disease implications in future therapy
    Journal of Molecular Neuroscience, 2003
    Co-Authors: Abraham Fisher, Michal Kligerspatz, Niva Natan, Hagar Sonego, Itzhak Marcovitch, Zipora Pittel, Rachel Haring, Nira Barner, Inbal Egozi, Rachel Brandeis
    Abstract:

    M1 muscarinic receptors (M1 mAChRs) play a role in an apparent linkage of three major hallmarks of Alzheimer's disease (AD): beta-amyloid (Abeta) peptide; tau hyperphosphorylation and paired helical filaments (PHFs); and loss of cholinergic function conducive to cognitive impairments. We evaluated the M1 muscarinic agonists AF102B (Cevimeline, EVOXAC trade mark : prescribed for Sjogren's syndrome), AF150(S), and AF267B on some of these hallmarks of AD. Activation of M1 mAChRs with these agonists leads, inter alia, to enhanced secretion of amyloid precursor protein (alpha-APP), (via alpha-secretase activation), to decreased Abeta (via gamma-secretase inhibition), and to inhibition of Abeta- and/or oxidative stress-induced cell death. In several animal models mimicking different aspects of AD, these drugs restored cognitive impairments, and in select cases induced a decrease in brain Abeta elevation, with a high safety margin, following po administration. Notably, in mice with small hippocampi, unlike rivastigmine and nicotine, AF150(S) and AF267B restored cognitive impairments also on escape latency in a Morris water maze paradigm, in reversal learning. Studies from other labs showed that AF102B and talsaclidine (another M1 agonist) decreased cerbrospinal fluid (CSF) Abeta in AD patients following chronic treatment, being the first reported drugs with such a profile. The clinical significance of these studies remains to be elucidated, yet based on in vivo (rabbits) and in vitro studies (cell cultures), our M1 agonists can decrease brain Abeta, owing to a novel and dual complementary effect (e.g., inhibition of gamma-secretase and activation of alpha-secretase). Remarkably, although M1 agonists can decrease CSF Abeta in AD patients, an increased AD-type pathology in Parkinson's disease was recently been associated with chronic antimuscarinic treatment. In another aspect, these agonists decreased tau hyperphosphorylation in vitro and in vivo. Notably, nicotinic agonists or cholinesterase inhibitors increased tau hyperphosphorylation. In summary, the M1 agonists tested are effective on cognition and behavior and show unique disease-modifying properties owing to beneficial effects on major hallmarks of AD. This may place such drugs in the first line of modern AD therapies (e.g., beta- or gamma-secretase inhibitors, vaccines against Abeta, statins, and inhibitors of tau hyperphosphorylation).

  • af150 s and af267b m1 muscarinic agonists as innovative therapies for alzheimer s disease
    Journal of Molecular Neuroscience, 2002
    Co-Authors: Abraham Fisher, Rachel Brandeis, Rachel Haring Nira Barner, Michal Kligerspatz, Niva Natan, Hagar Sonego, Itzhak Marcovitch, Zipora Pittel
    Abstract:

    The M1 muscarinic agonists AF102B (Cevimeline, EVOXACTM: prescribed in USA and Japan for Sjogren’s Syndrome), AF150(S) and AF267B—1) are neurotrophic and synergistic with neurotrophins such as nerve growth factor and epidermal growth factor; 2) elevate the non-amyloidogenic amyloid precursor protein (α-APPs) in vitro and decrease β-amyloid (Aβ) levels in vitro and in vivo; and 3) inhibit Aβ- and oxidative-stress-induced cell death and apoptosis in PC12 cells transfected with the M1 muscarinic receptor. These effects can be combined with the beneficial effects of these compounds on some other major hallmarks of Alzheimer’s disease (AD) (e.g. τ hyperphosphorylation and paired helical filaments [PHF]; and loss of cholinergic function conducive to cognitive impairments.) These drugs restored cognitive impairments in several animal models for AD, mimicking different aspects of AD, with a high safety margin (e.g. AF150[S] >1500 and AF267B >4500). Notably, these compounds show a high bioavailability and a remarkable preference for the brain vs. plasma following po administration. In mice with small hippocampi, unlike rivastigmine and nicotine, AF150(S) and AF267B restored cognitive impairments also on escape latency in a Morris water maze paradigm in reversal learning. Furthermore, in aged and cognitively impaired microcebes (a natural animal model that mimics AD pathology and cognitive impairments), prolonged treatment with AF150(S) restored cognitive and behavioral impairments and decreased τ hyperphosphorylation, PHF and astrogliosis. Our M1 agonists, alone or in polypharmacy, may present a unique therapy in AD due to their beneficial effects on major hallmarks of AD.

  • Use of muscarinic agonists in the treatment of Sjögren's syndrome.
    Clinical immunology (Orlando Fla.), 2001
    Co-Authors: Robert I. Fox, Yrjö Konttinen, Abraham Fisher
    Abstract:

    Two muscarinic agonists (pilocarpine and Cevimeline) have recently been approved for the treatment of symptoms of xerostomia in Sjogren's syndrome (SS). These agents stimulate the M1 and M3 receptors present on salivary glands, leading to increased secretory function. The use of these agents emphasizes the importance of neuroendocrine mechanisms in SS, which is considered an autoimmune disorder. We review recent studies on the release of cytokines and metalloproteinases in SS-affected glands and their influence on the release of and response to neurotransmitters. Also, we review the structure and function of muscarinic receptors as they may relate to SS and the potential use of novel muscarinic agonists in SS.

Di Wang - One of the best experts on this subject based on the ideXlab platform.

  • Abnormal subcellular localization of AQP5 and downregulated AQP5 protein in parotid glands of streptozotocin-induced diabetic rats
    biochimica et biophysica acta general subjects, 2011
    Co-Authors: Di Wang, Yuan Zhenfang, Inoue Noriko, Cho Gota, Shono Masayuki, Ishikawa Yasuko
    Abstract:

    Background: The mechanisms underlying diabetic xerostomia have not been clarified in relation with aquaporin-5 (AQP5) subcellular localization in salivary glands. Methods: Western blotting, real-time PCR, and immunocytochemistry were used to analyse AQP5 protein levels and mRNA expression. AQP5 protein levels were measured in the apical plasma membrane (APM) and detergent-insoluble fraction prepared from streptozotocin-diabetic rat parotid glands. Results: Despite an increase in AQP5 mRNA, AQP5 protein levels were decreased in diabetic parotid glands compared with controls. Immunohistochemical studies indicated that AQP5, under unstimulated conditions, colocalised with flotillin-2 and GM1 with a diffuse pattern in the apical cytoplasm of acinar and duct cells in both control and diabetic rats. Ten minutes after intravenous injection of muscarinic agonist Cevimeline. AQP5 was dramatically increased together with flotillin-2 and GM1 in the APM of parotid acinar and duct cells of control but not diabetic rats. Sixty minutes after injection, AQP5 was located in a diffuse pattern in the apical cytoplasm in both rats. Treatment of the parotid tissues with Cevimeline for 10 min increased the Triton X-100 solubility of AQP5 in control but not diabetic rats. Administration of insulin to diabetic rats tended to restore the Cevimeline-induced translocation of AQP5. Conclusion: Lack of AQP5 translocation in the salivary gland in response to a muscarinic agonist and downregulation of AQP5 protein might lead to diabetic xerostomia. General significance: Cevimeline is useful to cure diabetic xerostomia under insulin administration. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000290067900007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyBiophysicsSCI(E)11ARTICLE5543-554181

  • identification of aquaporin 5 and lipid rafts in human resting saliva and their release into Cevimeline stimulated saliva
    Biochimica et Biophysica Acta, 2009
    Co-Authors: Yan Pan, Di Wang, Fusako Iwata, Masahiro Muraguchi, Keiko Ooga, Yasukazu Ohmoto, Masaaki Takai, Gota Cho, Jinsen Kang, Masayuki Shono
    Abstract:

    Abstract Background It is unknown whether AQP5 and lipid rafts are released into human unstimulated (resting) saliva and saliva in response to secretagogues. Methods In order to quantitate the salivary concentration of AQP5, we produced a polyclonal antibody for human AQP5 and developed an enzyme-like immunosorbent assay (ELISA). Results AQP5 and lipid rafts were identified in human resting saliva. The amount of AQP5 in resting saliva showed a diurnal variation with high levels during waking hours, and an age-related decrease in AQP5 was coincident with the volume of resting saliva. Cevimeline, a muscarinic acetylcholine receptor (mAChR) agonist, induced the release of AQP5 with lipid rafts, amylase, mucin, and lysozyme. Changes in saliva AQP5 levels after Cevimeline administration occurred simultaneously with changes in saliva flow rates. Confocal microscopy revealed that AQP5 was located in the apical plasma membrane and showed a diffuse pattern in parotid glands under resting conditions. Following Cevimeline administration, AQP5 was predominantly associated with the APM and was localized in the lumen. General significance AQP5 and lipid rafts were released with salivary proteins from human salivary glands by the stimulation of M 3 mAChRs, and that changes in saliva AQP5 levels can be used as an indicator of salivary flow rate and also as a useful index of M 3 mAChR agonist's action on human salivary glands.

  • Identification of aquaporin-5 and lipid rafts in human resting saliva and their release into Cevimeline-stimulated saliva
    biochimica et biophysica acta general subjects, 2009
    Co-Authors: Pan Yan, Di Wang, Cho Gota, Iwata Fusako, Muraguchi Masahiro, Ooga Keiko, Ohmoto Yasukazu, Takai Masaaki, Kang Jinsen, Shono Masayuki
    Abstract:

    Background: It is unknown whether AQP5 and lipid rafts are released into human unstimulated (resting) saliva and saliva in response to secretagogues. Methods: In order to quantitate the salivary concentration of AQP5, we produced a polyclonal antibody for human AQP5 and developed an enzyme-like immunosorbent assay (ELISA). Results: AQP5 and lipid rafts were identified in human resting saliva. The amount of AQP5 in resting saliva showed a diurnal variation with high levels during waking hours, and an age-related decrease in AQP5 was coincident with the volume of resting saliva. Cevimeline, a muscarinic acetylcholine receptor (mAChR) agonist, induced the release of AQP5 with lipid rafts, amylase, mucin, and lysozyme. Changes in saliva AQP5 levels after Cevimeline administration occurred simultaneously with changes in saliva flow rates. Confocal microscopy revealed that AQP5 was located in the apical plasma membrane and showed a diffuse pattern in parotid glands under resting conditions. Following Cevimeline administration, AQP5 was predominantly associated with the APM and was localized in the lumen. General significance: AQP5 and lipid rafts were released with salivary proteins from human salivary glands by the stimulation Of M(3) mAChRs, and that changes in saliva AQP5 levels can be used as an indicator of salivary flow rate and also as a useful index Of M3 mAChR agonist's action on human salivary glands. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000262307700007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyBiophysicsSCI(E)10ARTICLE149-56179

  • Correlation between salivary secretion and salivary AQP5 levels in health and disease.
    The journal of medical investigation : JMI, 2009
    Co-Authors: Di Wang, Fusako Iwata, Masahiro Muraguchi, Keiko Ooga, Yasukazu Ohmoto, Masaaki Takai, Toyoki Mori, Yasuko Ishikawa
    Abstract:

    Saliva samples are useful for noninvasive diagnosis of oral and systemic diseases. The water channel protein aquaporin-5 (AQP5) is released into human saliva. Salivary AQP5 levels show a diurnal variation with the secretion of high levels during the waking hours. An age-related decrease in salivary AQP5 levels parallels a decrease in the volume of saliva. Cevimeline, a muscarinic acetylcholine receptor (mAChR) agonist, induces the release of AQP5. Changes in salivary AQP5 levels after Cevimeline administration occur simultaneously with changes in saliva flow rate. AQP5 and lipid rafts are released separately from human salivary glands upon M(3) mAChR stimulation. In patients with diabetes mellitus or Sjögren's syndrome, a decrease in salivary secretion occurs concomitantly with low salivary AQP5 levels. Salivary AQP5 levels correlate with salivary secretion in both healthy and disease states, suggesting that changes in salivary AQP5 levels can be used as an indicator of salivary flow rate and the effect of M(3) mAChR agonists on human salivary glands.

Shono Masayuki - One of the best experts on this subject based on the ideXlab platform.

  • Abnormal subcellular localization of AQP5 and downregulated AQP5 protein in parotid glands of streptozotocin-induced diabetic rats
    biochimica et biophysica acta general subjects, 2011
    Co-Authors: Di Wang, Yuan Zhenfang, Inoue Noriko, Cho Gota, Shono Masayuki, Ishikawa Yasuko
    Abstract:

    Background: The mechanisms underlying diabetic xerostomia have not been clarified in relation with aquaporin-5 (AQP5) subcellular localization in salivary glands. Methods: Western blotting, real-time PCR, and immunocytochemistry were used to analyse AQP5 protein levels and mRNA expression. AQP5 protein levels were measured in the apical plasma membrane (APM) and detergent-insoluble fraction prepared from streptozotocin-diabetic rat parotid glands. Results: Despite an increase in AQP5 mRNA, AQP5 protein levels were decreased in diabetic parotid glands compared with controls. Immunohistochemical studies indicated that AQP5, under unstimulated conditions, colocalised with flotillin-2 and GM1 with a diffuse pattern in the apical cytoplasm of acinar and duct cells in both control and diabetic rats. Ten minutes after intravenous injection of muscarinic agonist Cevimeline. AQP5 was dramatically increased together with flotillin-2 and GM1 in the APM of parotid acinar and duct cells of control but not diabetic rats. Sixty minutes after injection, AQP5 was located in a diffuse pattern in the apical cytoplasm in both rats. Treatment of the parotid tissues with Cevimeline for 10 min increased the Triton X-100 solubility of AQP5 in control but not diabetic rats. Administration of insulin to diabetic rats tended to restore the Cevimeline-induced translocation of AQP5. Conclusion: Lack of AQP5 translocation in the salivary gland in response to a muscarinic agonist and downregulation of AQP5 protein might lead to diabetic xerostomia. General significance: Cevimeline is useful to cure diabetic xerostomia under insulin administration. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000290067900007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyBiophysicsSCI(E)11ARTICLE5543-554181

  • Identification of aquaporin-5 and lipid rafts in human resting saliva and their release into Cevimeline-stimulated saliva
    biochimica et biophysica acta general subjects, 2009
    Co-Authors: Pan Yan, Di Wang, Cho Gota, Iwata Fusako, Muraguchi Masahiro, Ooga Keiko, Ohmoto Yasukazu, Takai Masaaki, Kang Jinsen, Shono Masayuki
    Abstract:

    Background: It is unknown whether AQP5 and lipid rafts are released into human unstimulated (resting) saliva and saliva in response to secretagogues. Methods: In order to quantitate the salivary concentration of AQP5, we produced a polyclonal antibody for human AQP5 and developed an enzyme-like immunosorbent assay (ELISA). Results: AQP5 and lipid rafts were identified in human resting saliva. The amount of AQP5 in resting saliva showed a diurnal variation with high levels during waking hours, and an age-related decrease in AQP5 was coincident with the volume of resting saliva. Cevimeline, a muscarinic acetylcholine receptor (mAChR) agonist, induced the release of AQP5 with lipid rafts, amylase, mucin, and lysozyme. Changes in saliva AQP5 levels after Cevimeline administration occurred simultaneously with changes in saliva flow rates. Confocal microscopy revealed that AQP5 was located in the apical plasma membrane and showed a diffuse pattern in parotid glands under resting conditions. Following Cevimeline administration, AQP5 was predominantly associated with the APM and was localized in the lumen. General significance: AQP5 and lipid rafts were released with salivary proteins from human salivary glands by the stimulation Of M(3) mAChRs, and that changes in saliva AQP5 levels can be used as an indicator of salivary flow rate and also as a useful index Of M3 mAChR agonist's action on human salivary glands. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000262307700007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyBiophysicsSCI(E)10ARTICLE149-56179

Takayuki Sumida - One of the best experts on this subject based on the ideXlab platform.

  • generation and functional analysis of monoclonal antibodies against the second extracellular loop of human m3 muscarinic acetylcholine receptor
    Modern Rheumatology, 2012
    Co-Authors: Hiroto Tsuboi, Mana Iizuka, Isao Matsumoto, Yumi Nakamura, Naomi Matsuo, Takayuki Sumida
    Abstract:

    The M3 muscarinic acetylcholine receptor (M3R) plays a crucial role in the activation of salivary and lachrymal glands. The M3R contains four extracellular domains (the N-terminal, and the first, second, and third extracellular loops), and we recently detected antibodies against each of these four domains in a subgroup of patients with Sjogren’s syndrome (SS). Functional analysis indicated that the influence of such anti-M3R antibodies on salivary secretion might differ based on the epitopes to which they bind. To clarify the relationship between B-cell epitopes on the M3R and its function, we generated two hybridomas producing anti-M3R monoclonal antibodies against the second extracellular loop of M3R (anti-M3R2nd mAbs) and analyzed their function by Ca2+-influx assays, using a human salivary gland (HSG) cell line. These two anti-M3R2nd mAbs suppressed Ca2+-influx in the HSG cells induced by Cevimeline stimulation, suggesting that autoantibodies against the second extracellular loop of M3R could be involved in salivary dysfunction in patients with SS.

  • new epitopes and function of anti m3 muscarinic acetylcholine receptor antibodies in patients with sjogren s syndrome
    Clinical and Experimental Immunology, 2010
    Co-Authors: Hiroto Tsuboi, Mana Iizuka, Isao Matsumoto, Yumi Nakamura, Ei Wakamatsu, Taichi Hayashi, Daisuke Goto, Satoshi Ito, Takayuki Sumida
    Abstract:

    Summary M3 muscarinic acetylcholine receptor (M3R) plays a crucial role in the secretion of saliva from salivary glands. It is reported that some patients with Sjogren's syndrome (SS) carried inhibitory autoantibodies against M3R. The purpose of this study is to clarify the epitopes and function of anti-M3R antibodies in SS. We synthesized peptides encoding the extracellular domains of human-M3R including the N-terminal region and the first, second and third extracellular loops. Antibodies against these regions were examined by enzyme-linked immunosorbent assay in sera from 42 SS and 42 healthy controls. For functional analysis, human salivary gland (HSG) cells were preincubated with immunoglobulin G (IgG) separated from sera of anti-M3R antibody-positive SS, -negative SS and controls for 12 h. After loading with Fluo-3, HSG cells were stimulated with Cevimeline hydrochloride, and intracellular Ca2+ concentrations [(Ca2+)i] were measured. Antibodies to the N-terminal, first, second and third loops were detected in 42·9% (18 of 42), 47·6% (20 of 42), 54·8% (23 of 42) and 45·2% (19 of 42) of SS, while in 4·8% (two of 42), 7·1% (three of 42), 2·4% (one of 42) and 2·4% (one of 42) of controls, respectively. Antibodies to the second loop positive SS-IgG inhibited the increase of (Ca2+)i induced by Cevimeline hydrochloride. Antibodies to the N-terminal positive SS-IgG and antibodies to the first loop positive SS-IgG enhanced it, while antibodies to the third loop positive SS-IgG showed no effect on (Ca2+)i as well as anti-M3R antibody-negative SS-IgG. Our results indicated the presence of several B cell epitopes on M3R in SS. The influence of anti-M3R antibodies on salivary secretion might differ based on these epitopes.

Anna Greta Barbe - One of the best experts on this subject based on the ideXlab platform.

  • Medication-Induced Xerostomia and Hyposalivation in the Elderly: Culprits, Complications, and Management
    Drugs & Aging, 2018
    Co-Authors: Anna Greta Barbe
    Abstract:

    Medication-induced xerostomia and hyposalivation will increasingly become oral health issues for older and geriatric patients because of the likely high prevalence of medication intake and polypharmacy, with a complex negative impact on other symptoms such as dysphagia, caries incidence, malnutrition, and quality of life. All healthcare professionals are encouraged to investigate dry mouth symptoms among their patients, since diagnosis can easily be performed within daily clinical practice. This practical article also provides a review of available treatment options, which include medication changes towards products with fewer xerogenic side effects or dose reductions, if possible, as well as multidisciplinary, preventive care-oriented approaches that consider all influencing factors and treatment of the oral symptoms. In addition, several topical agents and saliva substitutes are discussed that may provide symptomatic relief but need to be carefully adapted to each patient’s situation in terms of usability and practicability and in the knowledge that therapeutic success varies with each individual. Innovative methods such as intraoral electrostimulation or topical application of anticholinesterase on the oral mucosa are also discussed. The most commonly prescribed pharmaceutical treatment options for dry mouth are pilocarpine (a parasympathomimetic agent with potent muscarinic, cholinergic salivation-stimulating properties) and Cevimeline (a quinuclidine analogue with therapeutic and side effects similar to those of pilocarpine). These pharmaceutic treatment options are described in the context of older patients, where the highly prevalent cholinergic side effects, which include nausea, emesis, bronchoconstriction, among others, need to be thoroughly supervised by the healthcare professionals involved. Providing these therapeutic options to patients with medication-induced dry mouth will help improve their oral health and therefore maintain a better quality of life, general health, and well-being.

  • long term use of the sialogogue medications pilocarpine and Cevimeline can reduce xerostomia symptoms and increase salivary flow in head and neck cancer survivors after radiotherapy
    Journal of Evidence Based Dental Practice, 2017
    Co-Authors: Anna Greta Barbe
    Abstract:

    Article Title and Bibliographic Information Interventions for the management of radiotherapy-induced xerostomia and hyposalivation: A systematic review and meta-analysis. Mercadante V, Hamad AA, Lodi G, Porter S, Fedele S. Oral Oncol 2017;66:64-74. Source of Funding The authors reported that no external funding sources directly supported this study Type of Study/Design Systematic review and meta-analysis