Retinal DegenerationPhase 1/2STARSAF02NCT01278277
Saffron Supplementation in Stargardt's Disease
A Phase 1/2 study testing Saffron supplementation in people with Retinal Degeneration and Genetic Disease, run by Catholic University of the Sacred Heart at 1 site in Italy.
Trial summary
The general area of research in which this project has been designed is that of retinal degeneration related to mutations in the ABCR gene, responsible of Stargardt disease/fundus flavimaculatus retinal dystrophy (STD/FF). STG/FF is one of the major causes of vision impairment in the young age. Read more about this study
- Who is it for?
- Ages 8 to 60 years
- Conditions the study is for
- Retinal Degeneration, Genetic Disease, Single-Gene Defects
- What is being tested?
- Saffron supplementation
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 30 participants
- Where
- 1 siteItaly
- Study dates
- Feb 2011to Dec 2017
- Phase
- Phase 1/2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 8 to 60 years
- All sexes
- No healthy volunteers
- Child, Adult
Who may be able to join
- Macular and peripheral retinal degeneration with typical funduscopic lesions (retinal flecks)
- Relatively preserved central retinal function
- Known genotype or genotype under study
Who cannot join
- absence of a rod-cone pattern of dysfunction
- acuity less than 0.1
- Unknown genotype
Trial locations and contacts
1 site in 1 country.
About this study
Official title: A Novel Therapeutic Strategy Targeting Photoreceptor Oxidative Damage in ABCR-related Retinal Degenerations
The general area of research in which this project has been designed is that of retinal degeneration related to mutations in the ABCR gene, responsible of Stargardt disease/fundus flavimaculatus retinal dystrophy (STD/FF). STG/FF is one of the major causes of vision impairment in the young age. STG/FF originates typically from the dysfunction and loss of cone and rod photoreceptors, developing through a photo-oxidative mechanism. The major disease locus is the central retina, i.e. the macula, whose neurons have the highest density and underlie critical functions such as visual acuity, color vision and contrast sensitivity. There is currently no cure for STG/FF. Recent experimental findings indicate that Saffron, derived from the pistils of Crocus Sativus, may have a role as a retinal neuro-protectant against oxidative damage. The stigmata of Crocus sativus contain biologically high concentrations of chemical compounds including crocin, crocetin, whose multiple C=C bonds provide the antioxidant potential. In addition it is well known that this compound is safe and free of adverse side effects. The aim of this research is to investigate the influence of short-term Saffron supplementation on retinal function in STG/FF patients carrying ABCR mutations. The macular cone-mediated electroretinogram (ERG) in response to high-frequency flicker (focal flicker ERG) will be employed as the main outcome variable. Secondary outcome variable will be the psychophysical cone system recovery after bleaching.
Read the detailed description
Research Plan Background Stargardt disease (STGD/FFM) is the most common hereditary recessive macular dystrophy (Blacharski, 1988) characterized by juvenile to young adult onset, central visual impairment, progressive bilateral atrophy of the macula and retinal pigment epithelium (RPE), with a frequent appearance of orange/yellow flecks distributed around the macula and/or the mid retinal periphery (Noble and Carr, 1971). A clinically similar retinal disorder, fundus flavimaculatus (FFM), often displays later ages of onset and slower progression. It has been suggested and demonstrated (Allikmets et al., 1997) that STGD and FFM represent allelic disorders. Mutations in the gene encoding an ATP-binding cassette (ABC) transporter (ABCR), mapping to chromosome 1p13-p21, have been found to be responsible of STGD (Allikmets et al., 1997). The ABCR gene is expressed exclusively and at high levels in the retina, in both rod and cone photoreceptors (Molday et al., 2000). A recent study by Weng et al. (1999) , investigating the molecular mechanisms underlying photoreceptor degeneration in ABCR knock-out mice, proposed that photoreceptors die as a consequence of 'poisoning' of the RPE by lipofuscin accumulation and loss of the RPE support role. Accumulation within the RPE cells of a compound, A2E, forming from condensation of phosphatydilethanlolamine and the all-trans-retinal released from photoactivated rhodopsin (Sparrow et al., 2000), probably leads in vivo to an increased absorption of blue lights and to phototoxic RPE cell damage. The mutation-induced disease may affect both rod and cone photoreceptors, at relatively early stages. In vitro studies (Sun and Nathans, 2001) also demonstrated that the ABCR itself is an efficient target of all-trans-retinal-mediated photooxidative damage.
Clinically, many reports have documented an abnormal functioning of both macular and peripheral cones, as well as rods, in STGD/FFM (Moloney et al., 1983; Lachapelle et al., 1990). There is also evidence (Lois et al., 2001) that STGD/FFM may be associated with different patterns of retinal dysfunction, with a selective involvement of macular function, or more widespread dysfunction involving cone and/or rod function, showing intrafamilial consistency. Characteristic abnormalities of dark adaptation (Aleman et al., 1999), involving a delayed post-bleach recovery, to the baseline sensitivity, of the last branch of the adaptation curve have been also described. Similar abnormalities in rod dark adaptation have been recently found in a mice heterozygous for a null mutation in the ABCR gene (Mata et al., 2001). Clinical evidence (Parisi et al., 2002) indicates that also the recovery of cone sensitivity after bleaching is severely impaired in STG/FF, suggesting that profoundly altered retinoid recycling, leading to photoxidative damage, specifically occurs in cone photoreceptors.
Recent experimental findings (Maccarone et al., 2008) indicate that Saffron, derived from the pistils of Crocus Sativus, may have a role as a retinal neuro-protectant against oxidative damage. Indeed, Saffron has been shown to be protective, for both morphology and function, in a rat model of light-induced photoreceptor degeneration. In this model, cell death is thought to result from oxidative stress induced by prolonged increase in oxygen tension and photooxidation. Saffron is an attractive candidate to be tested because the stigmata of Crocus sativus contain biologically high concentrations of interesting chemical compounds including crocin, crocetin (Giaccio, 2004), whose multiple C=C bonds give the antioxidant potential. Not to mention that its centuries-long use as spice, with no known ill effects increases the confidence in secure applicability. In addition it has been recently reported (Ochiai et al., 2007) that crocins are able to activate metabolic pathways to protect cells from apoptosis and to reduce light induced death in isolated photoreceptors (Laabich et al., 2006) , while crocetin (Giaccio, 2004) increases oxygen diffusivity through liquids, such as plasma. Considering the high metabolic rate of photoreceptors, the availability of oxygen may be a critical factor in protecting them from death. In addition, Kanakis et al. (Kanakis et al, 2007) showed that metabolites of antioxidant flavonoids bind directly to DNA and induce its partial conformation to beta-DNA, thereby protecting the cell from damage. Based on these observation it comes clear that Saffron extract does not act as a simple antioxidant. The peculiar characteristics of Saffron components support the hypothesis of an involvement of very different ways of action going from antioxidant activity to direct control of gene expression. These components may act in humans as protective agents against oxidative damage for the ageing retina, and may repair early photoreceptor damage associated with STG/FF, whose disease patho-physiology has been linked by experimental studies (Mata et al, 2001) to light-induced oxidative damage to the outer retina. In STG/FF eyes, at early disease stages, the normal number of cone photoreceptors is partially retained, although the cells might be dysfunctional. As a result of the rescuing effects of Saffron, the pool of damaged but viable photoreceptors could increase its response, resulting in improved retinal sensitivity.
The objective of the present project is to evaluate whether Saffron supplementation has a beneficial neuro-protective effect for the damaged retinas as consequence of ABCR mutation-STD/FF.
Clinical Protocol Patients A group of 30 STG/FF patients (14 males, 16 females, age range: 15-68 years) will be included in this study. Patients will meet the following inclusion criteria: 1. Macular and peripheral retinal degeneration with typical funduscopic lesions (retinal flecks) and a cone-rod pattern of retinal dysfunction, as determined by standard Ganzfeld electroretinography and dark-adapted fundus perimetry, and classic fundus appearance, 2. Relatively preserved central retinal function (visual field by Goldmann V/4e > 30°, corrected EDTRS visual acuity > 20/80) and stable central fixation as determined by a Visuskope, 3. Known genotype or genotype under study, 4. At least four follow-up clinical examination over the past three years, 5. No or minimal ocular media opacities, 6. No concomitant ocular (e.g. glaucoma, amblyopia) or systemic diseases. Informed consent for all patients and controls will be obtained after the aims and procedures of the study will be explained in detail.
Treatment and Testing Schedule The patients will be divided into two groups: 15 will treated with oral supplementation of a daily dose of Saffron for 90 days, and 15 will undergo placebo treatment during the same period. At the end of a 90 days period the patients will be crossed-over and assigned respectively to placebo or Saffron supplementation. In all patients, clinical examination, including visual acuity testing with a calibrated standard Snellen chart and fundus examination by direct and indirect ophthalmoscopy, and FERG testing will be performed at the study entry (baseline) and after 180 days of treatment or placebo. In all cases, compliance will be judged by telephone interview and pill counts. Adverse side effects will be reported.
Electrophysiological Methods FERG testing will be performed according to a previously published technique (Falsini et al., 2000). Briefly, ERGs will be elicited by the LED-generated sinusoidal luminance modulation of a circular uniform field (18° in diameter, 80 cd/m2 mean luminance, dominant wavelength: 630 nm), presented at the frequency of 41 Hz on the rear of a ganzfeld bowl, illuminated at the same mean luminance as the stimulus. A series of FERG responses will be collected at different modulation depths [quantified by the Michelson luminance contrast formula: 100%*(Lmax -Lmin)/(Lmax +Lmin), where Lmax and Lmin are maximum and minimum luminance, respectively] between 16.5% and 93.8% in 0.1 to 0.3 log unit steps. FERG signals will be acquired in sequence for six values of modulation depth between 16.5 to 93.5%, presented in an increasing order. For each patient FERG log amplitudes will be plotted as a function of log modulation depth. The resulting function's slope will be determined by a linear regression. From the same regression line, FERG threshold will be estimated from the value of log modulation depth yielding a criterion amplitude, corresponding to a S/N ratio of 3.
Psychophysics An increment threshold technique will be used to evaluate the recovery of cone system sensitivity after bleaching exposure. Psychophysical threshold will be determined at the paracentral visual field locations with preserved visual sensitivity, by presenting a 0.5 sec flashing light on a light adapting background of 20 cd/sqm. Following baseline assessment, the threshold intensity for the flashed light will be measured and plotted as a function of time, following 30 sec exposure to an adapting light (delivered in Maxwellian view by means of a calibrated indirect ophthalmoscope) whose intensity is estimated bleach approx 30% of the cone photopigment. The resulting dynamic recovery function, fitted by an exponential function, describes the sensitivity recovery of the photopic system following bleaching, and reflects either the rate of free opsin inactivation or photopigment synthesis. A computer-controlled system, employing a commercially available apparatus, has been developed (Fadda et al., 2001) for measuring bleaching adaptation of the cone system.
Statistical Analysis Sample size estimates of patients for this study will be based on previous investigations (Parisi et al., 2001) where the between- and within-subjects variability (expressed as data SD) of FERG parameters was determined in STG/FF patients. Assuming between- and within-subjects SDs in FERG amplitude and phase of 0.1 logmicroV and 20 degrees, respectively, the sample sizes of patients assigned to both Saffron and placebo provide a power of 80%, at an alpha = 0.05, for detecting in each group a test-retest difference (i.e. 90 days minus baseline test) of 0.1 logmicroV (SD: 0.1) and 30 degrees (SD: 20) in amplitude and phase, respectively. Results will be analyzed by multivariate statistics (multivariate analysis of variance for repeated measures, MANOVA). In all the analyses a p < 0.05 will be considered as statistically significant.
- Being tested
- Saffron supplementation, placebo
- Keywords
- Stargardt disease, macula, electroretinogram, saffron
- Medical subject headings
- Retinal Degeneration, Genetic Diseases, Inborn, Macular Degeneration, Stargardt Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Saffron supplementationDietary supplement
Also called Zaffit Special
Saffron supplementation 20 mg
placeboOther
placebo supplementation
| Study group | Role | What they receive |
|---|---|---|
| placebo supplementation | Placebo comparator | patients will be assigned, in a cross-over design, to placebo or supplement administration Receives: Other: placebo |
| Saffron | Active comparator | Saffron Supplementation 20 mg/die Receives: Dietary Supplement: Saffron supplementation |
What is being measured
The primary outcome is the main question the study is designed to answer.
Focal electroretinogram (FERG)
ERGs will be elicited by the LED-generated sinusoidal luminance modulation of a circular uniform field (18° in diameter, 80 cd/m2 mean luminance, dominant wavelength: 630 nm), presented at the frequency of 41 Hz on the rear of a ganzfeld bowl, illuminated at the same mean luminance as the stimulus.
Measured: six months
Secondary outcomes (1)
Psychophysical recovery of cone system sensitivity after bleaching
Psychophysical threshold will be determined at the paracentral visual field locations with preserved visual sensitivity, by presenting a 0.5 sec flashing light on a light adapting background of 20 cd/sqm. Following baseline assessment, the threshold intensity for the flashed light will be measured and plotted as a function of time, following 30 sec exposure to an adapting light (delivered in Maxwellian view by means of a calibrated indirect ophthalmoscope) whose intensity is estimated bleach approx 30% of the cone photopigment.
Measured: six months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted17 Jan 2011 (estimated)
- Study startFeb 2011
- Primary completionNov 2017 (estimated)
- Study completionDec 2017 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (2)Papers the sponsor has linked to this study.
- Other trials for Retinal DegenerationStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 1/2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 30 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Catholic University of the Sacred Heart
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Benedetto Falsini, Catholic University of the Sacred Heart
- Investigators
- Benedetto Falsini, MD, Principal investigator, Catholic University of the Sacred HeartMarco Piccardi, MD, Principal investigator, Catholic University of the Sacred HeartSilvia Bisti, PhD, Study director, University of L'Aquila
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01278277
- Sponsor's protocol ID
- STARSAF02
- Acronym
- STARSAF02
- Status last verified
- Jul 2017
- First submitted
- 14 Jan 2011
- Last updated
- 19 Jul 2017
- Results posted
- No
- Data monitoring committee
- No
Publications
Falsini B, Piccardi M, Minnella A, Savastano C, Capoluongo E, Fadda A, Balestrazzi E, Maccarone R, Bisti S. Influence of saffron supplementation on retinal flicker sensitivity in early age-related macular degeneration. Invest Ophthalmol Vis Sci. 2010 Dec;51(12):6118-24. doi: 10.1167/iovs.09-4995. Epub 2010 Aug 4.
PubMed 20688744Piccardi M, Fadda A, Martelli F, Marangoni D, Magli A, Minnella AM, Bertelli M, Di Marco S, Bisti S, Falsini B. Antioxidant Saffron and Central Retinal Function in ABCA4-Related Stargardt Macular Dystrophy. Nutrients. 2019 Oct 15;11(10):2461. doi: 10.3390/nu11102461.
PubMed 31618812
Study at a glance
From the registry record, last updated by the sponsor on 19 Jul 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A Novel Therapeutic Strategy Targeting Photoreceptor Oxidative Damage in ABCR-related Retinal Degenerations
- ClinicalTrials.gov ID
- NCT01278277
- Acronym / sponsor ID
- STARSAF02 / STARSAF02
- Keywords
- Stargardt disease, macula, electroretinogram, saffron
- Phase
- Phase 1/2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 30 participants (estimated)
- Lead sponsor
- Catholic University of the Sacred HeartUniversity, hospital or other
- Study start
- Feb 2011
- Primary completion
- Nov 2017 (estimated)
- Study completion
- Dec 2017 (estimated)
- First posted
- 17 Jan 2011 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The general area of research in which this project has been designed is that of retinal degeneration related to mutations in the ABCR gene, responsible of Stargardt disease/fundus flavimaculatus retinal dystrophy (STD/FF). STG/FF is one of the major causes of vision impairment in the young age. STG/FF originates typically from the dysfunction and loss of cone and rod photoreceptors, developing through a photo-oxidative mechanism. The major disease locus is the central retina, i.e. the macula, whose neurons have the highest density and underlie critical functions such as visual acuity, color vision and contrast sensitivity. There is currently no cure for STG/FF. Recent experimental findings indicate that Saffron, derived from the pistils of Crocus Sativus, may have a role as a retinal neuro-protectant against oxidative damage. The stigmata of Crocus sativus contain biologically high concentrations of chemical compounds including crocin, crocetin, whose multiple C=C bonds provide the antioxidant potential. In addition it is well known that this compound is safe and free of adverse side effects. The aim of this research is to investigate the influence of short-term Saffron supplementation on retinal function in STG/FF patients carrying ABCR mutations. The macular cone-mediated electroretinogram (ERG) in response to high-frequency flicker (focal flicker ERG) will be employed as the main outcome variable. Secondary outcome variable will be the psychophysical cone system recovery after bleaching.
Detailed description
Research Plan Background Stargardt disease (STGD/FFM) is the most common hereditary recessive macular dystrophy (Blacharski, 1988) characterized by juvenile to young adult onset, central visual impairment, progressive bilateral atrophy of the macula and retinal pigment epithelium (RPE), with a frequent appearance of orange/yellow flecks distributed around the macula and/or the mid retinal periphery (Noble and Carr, 1971). A clinically similar retinal disorder, fundus flavimaculatus (FFM), often displays later ages of onset and slower progression. It has been suggested and demonstrated (Allikmets et al., 1997) that STGD and FFM represent allelic disorders. Mutations in the gene encoding an ATP-binding cassette (ABC) transporter (ABCR), mapping to chromosome 1p13-p21, have been found to be responsible of STGD (Allikmets et al., 1997). The ABCR gene is expressed exclusively and at high levels in the retina, in both rod and cone photoreceptors (Molday et al., 2000). A recent study by Weng et al. (1999) , investigating the molecular mechanisms underlying photoreceptor degeneration in ABCR knock-out mice, proposed that photoreceptors die as a consequence of 'poisoning' of the RPE by lipofuscin accumulation and loss of the RPE support role. Accumulation within the RPE cells of a compound, A2E, forming from condensation of phosphatydilethanlolamine and the all-trans-retinal released from photoactivated rhodopsin (Sparrow et al., 2000), probably leads in vivo to an increased absorption of blue lights and to phototoxic RPE cell damage. The mutation-induced disease may affect both rod and cone photoreceptors, at relatively early stages. In vitro studies (Sun and Nathans, 2001) also demonstrated that the ABCR itself is an efficient target of all-trans-retinal-mediated photooxidative damage.
Clinically, many reports have documented an abnormal functioning of both macular and peripheral cones, as well as rods, in STGD/FFM (Moloney et al., 1983; Lachapelle et al., 1990). There is also evidence (Lois et al., 2001) that STGD/FFM may be associated with different patterns of retinal dysfunction, with a selective involvement of macular function, or more widespread dysfunction involving cone and/or rod function, showing intrafamilial consistency. Characteristic abnormalities of dark adaptation (Aleman et al., 1999), involving a delayed post-bleach recovery, to the baseline sensitivity, of the last branch of the adaptation curve have been also described. Similar abnormalities in rod dark adaptation have been recently found in a mice heterozygous for a null mutation in the ABCR gene (Mata et al., 2001). Clinical evidence (Parisi et al., 2002) indicates that also the recovery of cone sensitivity after bleaching is severely impaired in STG/FF, suggesting that profoundly altered retinoid recycling, leading to photoxidative damage, specifically occurs in cone photoreceptors.
Recent experimental findings (Maccarone et al., 2008) indicate that Saffron, derived from the pistils of Crocus Sativus, may have a role as a retinal neuro-protectant against oxidative damage. Indeed, Saffron has been shown to be protective, for both morphology and function, in a rat model of light-induced photoreceptor degeneration. In this model, cell death is thought to result from oxidative stress induced by prolonged increase in oxygen tension and photooxidation. Saffron is an attractive candidate to be tested because the stigmata of Crocus sativus contain biologically high concentrations of interesting chemical compounds including crocin, crocetin (Giaccio, 2004), whose multiple C=C bonds give the antioxidant potential. Not to mention that its centuries-long use as spice, with no known ill effects increases the confidence in secure applicability. In addition it has been recently reported (Ochiai et al., 2007) that crocins are able to activate metabolic pathways to protect cells from apoptosis and to reduce light induced death in isolated photoreceptors (Laabich et al., 2006) , while crocetin (Giaccio, 2004) increases oxygen diffusivity through liquids, such as plasma. Considering the high metabolic rate of photoreceptors, the availability of oxygen may be a critical factor in protecting them from death. In addition, Kanakis et al. (Kanakis et al, 2007) showed that metabolites of antioxidant flavonoids bind directly to DNA and induce its partial conformation to beta-DNA, thereby protecting the cell from damage. Based on these observation it comes clear that Saffron extract does not act as a simple antioxidant. The peculiar characteristics of Saffron components support the hypothesis of an involvement of very different ways of action going from antioxidant activity to direct control of gene expression. These components may act in humans as protective agents against oxidative damage for the ageing retina, and may repair early photoreceptor damage associated with STG/FF, whose disease patho-physiology has been linked by experimental studies (Mata et al, 2001) to light-induced oxidative damage to the outer retina. In STG/FF eyes, at early disease stages, the normal number of cone photoreceptors is partially retained, although the cells might be dysfunctional. As a result of the rescuing effects of Saffron, the pool of damaged but viable photoreceptors could increase its response, resulting in improved retinal sensitivity.
The objective of the present project is to evaluate whether Saffron supplementation has a beneficial neuro-protective effect for the damaged retinas as consequence of ABCR mutation-STD/FF.
Clinical Protocol Patients A group of 30 STG/FF patients (14 males, 16 females, age range: 15-68 years) will be included in this study. Patients will meet the following inclusion criteria: 1. Macular and peripheral retinal degeneration with typical funduscopic lesions (retinal flecks) and a cone-rod pattern of retinal dysfunction, as determined by standard Ganzfeld electroretinography and dark-adapted fundus perimetry, and classic fundus appearance, 2. Relatively preserved central retinal function (visual field by Goldmann V/4e > 30°, corrected EDTRS visual acuity > 20/80) and stable central fixation as determined by a Visuskope, 3. Known genotype or genotype under study, 4. At least four follow-up clinical examination over the past three years, 5. No or minimal ocular media opacities, 6. No concomitant ocular (e.g. glaucoma, amblyopia) or systemic diseases. Informed consent for all patients and controls will be obtained after the aims and procedures of the study will be explained in detail.
Treatment and Testing Schedule The patients will be divided into two groups: 15 will treated with oral supplementation of a daily dose of Saffron for 90 days, and 15 will undergo placebo treatment during the same period. At the end of a 90 days period the patients will be crossed-over and assigned respectively to placebo or Saffron supplementation. In all patients, clinical examination, including visual acuity testing with a calibrated standard Snellen chart and fundus examination by direct and indirect ophthalmoscopy, and FERG testing will be performed at the study entry (baseline) and after 180 days of treatment or placebo. In all cases, compliance will be judged by telephone interview and pill counts. Adverse side effects will be reported.
Electrophysiological Methods FERG testing will be performed according to a previously published technique (Falsini et al., 2000). Briefly, ERGs will be elicited by the LED-generated sinusoidal luminance modulation of a circular uniform field (18° in diameter, 80 cd/m2 mean luminance, dominant wavelength: 630 nm), presented at the frequency of 41 Hz on the rear of a ganzfeld bowl, illuminated at the same mean luminance as the stimulus. A series of FERG responses will be collected at different modulation depths [quantified by the Michelson luminance contrast formula: 100%*(Lmax -Lmin)/(Lmax +Lmin), where Lmax and Lmin are maximum and minimum luminance, respectively] between 16.5% and 93.8% in 0.1 to 0.3 log unit steps. FERG signals will be acquired in sequence for six values of modulation depth between 16.5 to 93.5%, presented in an increasing order. For each patient FERG log amplitudes will be plotted as a function of log modulation depth. The resulting function's slope will be determined by a linear regression. From the same regression line, FERG threshold will be estimated from the value of log modulation depth yielding a criterion amplitude, corresponding to a S/N ratio of 3.
Psychophysics An increment threshold technique will be used to evaluate the recovery of cone system sensitivity after bleaching exposure. Psychophysical threshold will be determined at the paracentral visual field locations with preserved visual sensitivity, by presenting a 0.5 sec flashing light on a light adapting background of 20 cd/sqm. Following baseline assessment, the threshold intensity for the flashed light will be measured and plotted as a function of time, following 30 sec exposure to an adapting light (delivered in Maxwellian view by means of a calibrated indirect ophthalmoscope) whose intensity is estimated bleach approx 30% of the cone photopigment. The resulting dynamic recovery function, fitted by an exponential function, describes the sensitivity recovery of the photopic system following bleaching, and reflects either the rate of free opsin inactivation or photopigment synthesis. A computer-controlled system, employing a commercially available apparatus, has been developed (Fadda et al., 2001) for measuring bleaching adaptation of the cone system.
Statistical Analysis Sample size estimates of patients for this study will be based on previous investigations (Parisi et al., 2001) where the between- and within-subjects variability (expressed as data SD) of FERG parameters was determined in STG/FF patients. Assuming between- and within-subjects SDs in FERG amplitude and phase of 0.1 logmicroV and 20 degrees, respectively, the sample sizes of patients assigned to both Saffron and placebo provide a power of 80%, at an alpha = 0.05, for detecting in each group a test-retest difference (i.e. 90 days minus baseline test) of 0.1 logmicroV (SD: 0.1) and 30 degrees (SD: 20) in amplitude and phase, respectively. Results will be analyzed by multivariate statistics (multivariate analysis of variance for repeated measures, MANOVA). In all the analyses a p < 0.05 will be considered as statistically significant.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| placebo supplementation | Placebo comparator | Other: placebopatients will be assigned, in a cross-over design, to placebo or supplement administration |
| Saffron | Active comparator | Dietary Supplement: Saffron supplementationSaffron Supplementation 20 mg/die |
Who may qualify
- Ages
- 8 to 60 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult
Key inclusion criteria (3 listed)
- Macular and peripheral retinal degeneration with typical funduscopic lesions (retinal flecks)
- Relatively preserved central retinal function
- Known genotype or genotype under study
Key exclusion criteria (3 listed)
- absence of a rod-cone pattern of dysfunction
- acuity less than 0.1
- Unknown genotype
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Saffron supplementationAlso: Zaffit SpecialSaffron supplementation 20 mg | Dietary supplement | Saffron |
| placeboplacebo supplementation | Other | placebo supplementation |
Primary outcome
Focal electroretinogram (FERG)
Time frame: six months
ERGs will be elicited by the LED-generated sinusoidal luminance modulation of a circular uniform field (18° in diameter, 80 cd/m2 mean luminance, dominant wavelength: 630 nm), presented at the frequency of 41 Hz on the rear of a ganzfeld bowl, illuminated at the same mean luminance as the stimulus.
1 secondary outcome
Psychophysical recovery of cone system sensitivity after bleaching
Time frame: six months
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 19 Jul 2017.
- Background: PubMed 20688744Falsini B, Piccardi M, Minnella A, Savastano C, Capoluongo E, Fadda A, Balestrazzi E, Maccarone R, Bisti S. Influence of saffron supplementation on retinal flicker sensitivity in early age-related macular degeneration. Invest Ophthalmol Vis Sci. 2010 Dec;51(12):6118-24. doi: 10.1167/iovs.09-4995. Epub 2010 Aug 4.
- Derived from this study: PubMed 31618812Piccardi M, Fadda A, Martelli F, Marangoni D, Magli A, Minnella AM, Bertelli M, Di Marco S, Bisti S, Falsini B. Antioxidant Saffron and Central Retinal Function in ABCA4-Related Stargardt Macular Dystrophy. Nutrients. 2019 Oct 15;11(10):2461. doi: 10.3390/nu11102461.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Benedetto Falsini, MD principal investigator
Catholic University of the Sacred Heart
Marco Piccardi, MD principal investigator
Catholic University of the Sacred Heart
Silvia Bisti, PhD study director
University of L'Aquila
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 1/2 study testing Saffron supplementation in people with Retinal Degeneration and Genetic Disease, run by Catholic University of the Sacred Heart at 1 site in Italy.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 19 Jul 2017. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this combined phase mean?
Phase 1 studies test a treatment in a small group of people for the first time or in a new way, mainly to check safety and find the right dose.
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Focal electroretinogram (FERG) (time frame: six months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01278277, which also lists 2 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 19 Jul 2017.