Alzheimer DiseaseNCT05475158
Comparison of OCTA Factors in Patients With or Without Amyloid Pathology: A Prospective Study
An observational study of Alzheimer Disease and Amyloid Angiopathy, run by Pusan National University Hospital at 1 site in South Korea.
Trial summary
To compare alternation of retinal microcirculation within the macula and optic disc in patients with dementia, mild cognitive impairment (MCI), and cognitively healthy subjects who had positive amyloid biomarkers (Aβ +) or not, using optical coherence tomography angiography (OCTA). Read more about this study
- Who is it for?
- Ages 50 to 90 yearsHealthy volunteers can take part
- Conditions the study is for
- Alzheimer Disease, Amyloid Angiopathy, Macular Ischemia
- How many people
- 117 participants
- Where
- 1 siteSouth Korea
- Study dates
- 1 Sep 2019to 31 Jul 2021
- Phase
- Observational
- 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 50 to 90 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Neurologic Clinic of Pusan National University Hospital
Who may be able to join
- Clinical and pathologic diagnosis of ADD or MCI as well as cognitively unimpaired control (CU) from the Neurologic Clinic of Pusan National University Hospital
Who cannot join
- Patient not within the ages of 50-90 years old
- Patient with glaucoma, macular degeneration, retinal vascular disease including diabetic retinopathy, retinal vein occlusion
- Intraocular pressure (IOP) ≥ 21 mmHg
- Dense corneal or ocular media opacity
- History of ocular trauma or associated ocular disease
- Astigmatism ≥ 3.0 diopter or spherical equivalent ≥ 6.0 diopter
Show all 9Show fewer
- Best corrected visual acuity (BCVA) < 20/40
- Any ocular surgery except uncomplicated cataract extraction
- Uncontrolled hypertension and diabetes
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Comparison of Optical Coherence Tomography Angiographic Factors of Macula and Optic Disc in Patients With or Without Amyloid Pathology: A Prospective Study
To compare alternation of retinal microcirculation within the macula and optic disc in patients with dementia, mild cognitive impairment (MCI), and cognitively healthy subjects who had positive amyloid biomarkers (Aβ +) or not, using optical coherence tomography angiography (OCTA).
Read the detailed description
Alzheimer disease dementia (ADD) is the most common neurodegenerative disease dementia in elderly population associated with the accumulation of beta-amyloid (Aβ) plaques and tau neurofibrillary tangles (NFTs). Diagnostic biomarkers reflecting underlying amyloid or tau pathology of ADD have actively been developed. Of these, amyloid or tau positron emission tomography (PET) imaging and cerebrospinal fluid (CSF) Aβ1-42 or phosphorylated tau are representative biomarkers for ADD. However, these tend to be expensive, invasive, or available only in a tertiary hospital or a specialized laboratory. Alternative biomarkers which are inexpensive, less invasive, and highly available could be needed.
Patients with ADD commonly show visuospatial dysfunction which is mainly attributed to damage of parieto-occipital or temporo-occipital visual pathway. In addition, previous studies using optical coherence tomography (OCT) which is a useful tool measuring retinal nerve fiber layer thickness (RNFLT), macula ganglion cell/inner plexiform layer thickness (GC/IPLT) reported impaired pregeniculate afferent visual pathway, for example, reduction of RNFLT and loss of retinal ganglionic cells (RGCs) in patients with ADD.
The retina and brain have the same embryological origin. These were branched off from the forebrain, so the brain and retina have similar anatomic and physiologic traits of the vasculature. In line with this, several studies using laser doppler ultrasonography, or retinal function imager (RFI) revealed narrowed central retinal vein and decreased its blood velocity, or low blood flow rate of retinal arterioles and venules in patients with mild cognitive impairment (MCI) and ADD. The authors suggested that in patients with ADD, accumulation of Aβ in the vessel walls could cause disruption of basement membrane and endothelium, leading to the decreased vascular lumen and density of retinal vessel. Indeed, postmortem study revealed accumulated Aβ inside or around RGCs in AD.
OCTA can clearly visualize not only the specific layers of retinal vasculatures, including superficial, middle, and deep capillary plexuses, but also choroidal vessels with a high resolution and in a reproducible manner, without contrast agent. A few prior studies using OCTA reported enlarged foveal avascular zone (FAZ) and decrease of retinal vascular density and choroidal thickness in ADD or MCI compared to controls. On the other hand, the others showed no differences in FAZ area and vessel density between them.
In this study, the investigators first evaluated structural and microvascular changes of retina and the microvascular change of macula and optic disc in patients with clinically diagnosed ADD, MCI and cognitively normal controls using OCT and OCTA. Then, to investigate whether impaired pregeniculate visual pathway is truly associated with underlying amyloid pathology, the investigators further investigated those OCT and OCTA parameters in each subgroup with positive or negative amyloid biomarker.
- Conditions
- Alzheimer Disease, Amyloid Angiopathy, Macular Ischemia, Dementia, Mild Cognitive Impairment
- Keywords
- Alzheimer disease dementia, Mild cognitive impairment, Amyloid pathology, Optical coherence tomographic angiography
- Medical subject headings
- Alzheimer Disease, Amyloid angiopathy, Dementia, Cognitive Dysfunction
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Dementia | Patients with Alzheimer disease dementia (ADD) fulfilled the NIA-AA core clinical criteria for probable ADD and Aβ positive according to ATN classification scheme. Aβ positive refers to Aβ pathology (CSF Aβ1-42 < 631.8 pg/ml or positive amyloid deposits on 18F-flutemetamol PET by visual inspection). | |
| MCI (Mild cognitive impairment) | Patients with mild cognitive impairment (MCI) met the Petersen's criteria. | |
| CU (Cognitively unimpaired control) | CU consisted of cognitively unimpaired subjects whose cognition (as defined by the Seoul Neuropsychological Screening Battery (SNSB)) was within normal limits. | |
| Aβ positive | Aβ positive refers to Aβ pathology (CSF Aβ1-42 < 631.8 pg/ml or positive amyloid deposits on 18F-flutemetamol PET by visual inspection). | |
| Aβ negative | Aβ negative was within normal limits. |
What is being measured
The primary outcome is the main question the study is designed to answer.
SD-OCT imaging
Measuring macular GC/IPLT (μm) and cimcumpapillary RNFLT (μm).
The average, minimum, and 6 sectoral (superotemporal, superior, superonasal, inferonasal, inferior, and inferotemporal) GC/IPLT (μm) values are obtained.
The average, 4 sectoral (temporal, superior, nasal, and inferior), and 12 clock-hour circumpapillary RNFLT (μm) are obtained.
Multiple measurements will not be aggregated, but analyzed respectively.
Measured: Through study completion, measured at enrollment and analyzed from September 2019 to July 2021
SD-OCTA imaging
Acquiring microvasculature images of macular (6 × 6 mm^2 scan) and optic disc areas (4.5 × 4.5 mm^2 scan).
The average vessel density (VD, mm/mm^2) and perfusion density (PD, %) were automatically measured in the Early Treatment of Diabetic Retinopathy Study (ETDRS) grid with values shown in the nine subfields, central, inner, outer and full region.
The software calculated the area (mm^2), perimeter (mm), and circularity (defined as 4πA/P^2, where A was the area and P was the perimeter) of foveal avascular zone (FAZ). A circularity closer to 0 means an irregular shape, and closure to 1 indicates a circular shape.
Multiple measurements will not be aggregated, but analyzed respectively.
Measured: Through study completion, measured at enrollment and analyzed from September 2019 to July 2021
Secondary outcomes (2)
Diagnostic performance
Diagnostic performance of OCT and OCTA parameters according to underlying Aβpathology.
Receiver operating characteristic (ROC) curves were drawn by plotting sensitivity against 1-specificity, and areas under ROC curves (AUCs) were used to evaluate the diagnostic performance of continuous OCT/OCTA variables. Ideal cut-off points were derived using the Youden index
Measured: Through study completion, analyzed from July 2021 to July 2022
Correlations
Correlations between MMSE score and all of OCT/OCTA parameters were expressed as Pearson's or Spearman's rank correlation coefficients to account for the normal or non-normal distribution of the parameters, respectively.
OCT/OCTA parameters including as follows;
- macular GC/IPLT (μm): average, minimum, and 6 sectoral (superotemporal, superior, superonasal, inferonasal, inferior, and inferotemporal) GC/IPLT
- cimcumpapillary RNFLT (μm): verage, 4 sectoral (temporal, superior, nasal, and inferior), and 12 clock-hour circumpapillary RNFLT
- Macular vessel density (VD, mm/mm^2) \& perfusion density (PD, %) : VDs and PDs of central, parafoveal (nasal, temporal, superior, inferior), perifoveal (nasal, temporal, superior, inferior), and total
- Optic disc perfusion density (%) and flux index (from 0 to 1) : nasal, temporal, superior, inferior
Measured: Through study completion, analyzed from July 2021 to July 2022
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 Jul 2022
- Study start1 Sep 2019
- Primary completion31 Jul 2021
- Study completion31 Jul 2021
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (24)Papers the sponsor has linked to this study.
- Other trials for Alzheimer DiseaseStudies 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 117 participants (actual)
Sponsor and investigators
- Lead sponsor
- Pusan National University Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Eun-Joo Kim, MD, PhD, Principal investigator, Department of Neurology, Pusan National University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05475158
- Sponsor's protocol ID
- 1908-004-081
- Status last verified
- Jul 2022
- First submitted
- 23 Jun 2022
- Last updated
- 26 Jul 2022
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Arvanitakis Z, Shah RC, Bennett DA. Diagnosis and Management of Dementia: Review. JAMA. 2019 Oct 22;322(16):1589-1599. doi: 10.1001/jama.2019.4782.
PubMed 31638686Villemagne VL, Burnham S, Bourgeat P, Brown B, Ellis KA, Salvado O, Szoeke C, Macaulay SL, Martins R, Maruff P, Ames D, Rowe CC, Masters CL; Australian Imaging Biomarkers and Lifestyle (AIBL) Research Group. Amyloid beta deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study. Lancet Neurol. 2013 Apr;12(4):357-67. doi: 10.1016/S1474-4422(13)70044-9. Epub 2013 Mar 8.
PubMed 23477989Clark CM, Pontecorvo MJ, Beach TG, Bedell BJ, Coleman RE, Doraiswamy PM, Fleisher AS, Reiman EM, Sabbagh MN, Sadowsky CH, Schneider JA, Arora A, Carpenter AP, Flitter ML, Joshi AD, Krautkramer MJ, Lu M, Mintun MA, Skovronsky DM; AV-45-A16 Study Group. Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-beta plaques: a prospective cohort study. Lancet Neurol. 2012 Aug;11(8):669-78. doi: 10.1016/S1474-4422(12)70142-4. Epub 2012 Jun 28.
PubMed 22749065Albert MS, DeKosky ST, Dickson D, Dubois B, Feldman HH, Fox NC, Gamst A, Holtzman DM, Jagust WJ, Petersen RC, Snyder PJ, Carrillo MC, Thies B, Phelps CH. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-9. doi: 10.1016/j.jalz.2011.03.008. Epub 2011 Apr 21.
PubMed 21514249Grossman I, Lutz MW, Crenshaw DG, Saunders AM, Burns DK, Roses AD. Alzheimer's disease: diagnostics, prognostics and the road to prevention. EPMA J. 2010 Jun;1(2):293-303. doi: 10.1007/s13167-010-0024-3. Epub 2010 Jun 29.
PubMed 21124753Kirby E, Bandelow S, Hogervorst E. Visual impairment in Alzheimer's disease: a critical review. J Alzheimers Dis. 2010;21(1):15-34. doi: 10.3233/JAD-2010-080785.
PubMed 20182034Hodges JR. Alzheimer's centennial legacy: origins, landmarks and the current status of knowledge concerning cognitive aspects. Brain. 2006 Nov;129(Pt 11):2811-22. doi: 10.1093/brain/awl275.
PubMed 17071920Cronin-Golomb A, Corkin S, Rizzo JF, Cohen J, Growdon JH, Banks KS. Visual dysfunction in Alzheimer's disease: relation to normal aging. Ann Neurol. 1991 Jan;29(1):41-52. doi: 10.1002/ana.410290110.
PubMed 1996878Blanks JC, Hinton DR, Sadun AA, Miller CA. Retinal ganglion cell degeneration in Alzheimer's disease. Brain Res. 1989 Nov 6;501(2):364-72. doi: 10.1016/0006-8993(89)90653-7.
PubMed 2819446Sadun AA, Bassi CJ. Optic nerve damage in Alzheimer's disease. Ophthalmology. 1990 Jan;97(1):9-17. doi: 10.1016/s0161-6420(90)32621-0.
PubMed 2314849Jiang H, Liu Y, Wei Y, Shi Y, Wright CB, Sun X, Rundek T, Baumel BS, Landman J, Wang J. Impaired retinal microcirculation in patients with Alzheimer's disease. PLoS One. 2018 Feb 2;13(2):e0192154. doi: 10.1371/journal.pone.0192154. eCollection 2018.
PubMed 29394263Brown WR, Thore CR. Review: cerebral microvascular pathology in ageing and neurodegeneration. Neuropathol Appl Neurobiol. 2011 Feb;37(1):56-74. doi: 10.1111/j.1365-2990.2010.01139.x.
PubMed 20946471Feke GT, Hyman BT, Stern RA, Pasquale LR. Retinal blood flow in mild cognitive impairment and Alzheimer's disease. Alzheimers Dement (Amst). 2015 Apr 23;1(2):144-51. doi: 10.1016/j.dadm.2015.01.004. eCollection 2015 Jun.
PubMed 27239502Berisha F, Feke GT, Trempe CL, McMeel JW, Schepens CL. Retinal abnormalities in early Alzheimer's disease. Invest Ophthalmol Vis Sci. 2007 May;48(5):2285-9. doi: 10.1167/iovs.06-1029.
PubMed 17460292Wu J, Zhang X, Azhati G, Li T, Xu G, Liu F. Retinal microvascular attenuation in mental cognitive impairment and Alzheimer's disease by optical coherence tomography angiography. Acta Ophthalmol. 2020 Sep;98(6):e781-e787. doi: 10.1111/aos.14381. Epub 2020 Mar 9.
PubMed 32153141
Study at a glance
From the registry record, last updated by the sponsor on 26 Jul 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Comparison of Optical Coherence Tomography Angiographic Factors of Macula and Optic Disc in Patients With or Without Amyloid Pathology: A Prospective Study
- ClinicalTrials.gov ID
- NCT05475158
- Acronym / sponsor ID
- 1908-004-081
- Conditions
- Alzheimer Disease, Amyloid Angiopathy, Macular Ischemia, Dementia, Mild Cognitive Impairment
- Keywords
- Alzheimer disease dementia, Mild cognitive impairment, Amyloid pathology, Optical coherence tomographic angiography
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 117 participants (actual)
- Lead sponsor
- Pusan National University HospitalUniversity, hospital or other
- Study start
- 1 Sep 2019 (actual)
- Primary completion
- 31 Jul 2021 (actual)
- Study completion
- 31 Jul 2021 (actual)
- First posted
- 26 Jul 2022 (actual)
- 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.
To compare alternation of retinal microcirculation within the macula and optic disc in patients with dementia, mild cognitive impairment (MCI), and cognitively healthy subjects who had positive amyloid biomarkers (Aβ +) or not, using optical coherence tomography angiography (OCTA).
Detailed description
Alzheimer disease dementia (ADD) is the most common neurodegenerative disease dementia in elderly population associated with the accumulation of beta-amyloid (Aβ) plaques and tau neurofibrillary tangles (NFTs). Diagnostic biomarkers reflecting underlying amyloid or tau pathology of ADD have actively been developed. Of these, amyloid or tau positron emission tomography (PET) imaging and cerebrospinal fluid (CSF) Aβ1-42 or phosphorylated tau are representative biomarkers for ADD. However, these tend to be expensive, invasive, or available only in a tertiary hospital or a specialized laboratory. Alternative biomarkers which are inexpensive, less invasive, and highly available could be needed.
Patients with ADD commonly show visuospatial dysfunction which is mainly attributed to damage of parieto-occipital or temporo-occipital visual pathway. In addition, previous studies using optical coherence tomography (OCT) which is a useful tool measuring retinal nerve fiber layer thickness (RNFLT), macula ganglion cell/inner plexiform layer thickness (GC/IPLT) reported impaired pregeniculate afferent visual pathway, for example, reduction of RNFLT and loss of retinal ganglionic cells (RGCs) in patients with ADD.
The retina and brain have the same embryological origin. These were branched off from the forebrain, so the brain and retina have similar anatomic and physiologic traits of the vasculature. In line with this, several studies using laser doppler ultrasonography, or retinal function imager (RFI) revealed narrowed central retinal vein and decreased its blood velocity, or low blood flow rate of retinal arterioles and venules in patients with mild cognitive impairment (MCI) and ADD. The authors suggested that in patients with ADD, accumulation of Aβ in the vessel walls could cause disruption of basement membrane and endothelium, leading to the decreased vascular lumen and density of retinal vessel. Indeed, postmortem study revealed accumulated Aβ inside or around RGCs in AD.
OCTA can clearly visualize not only the specific layers of retinal vasculatures, including superficial, middle, and deep capillary plexuses, but also choroidal vessels with a high resolution and in a reproducible manner, without contrast agent. A few prior studies using OCTA reported enlarged foveal avascular zone (FAZ) and decrease of retinal vascular density and choroidal thickness in ADD or MCI compared to controls. On the other hand, the others showed no differences in FAZ area and vessel density between them.
In this study, the investigators first evaluated structural and microvascular changes of retina and the microvascular change of macula and optic disc in patients with clinically diagnosed ADD, MCI and cognitively normal controls using OCT and OCTA. Then, to investigate whether impaired pregeniculate visual pathway is truly associated with underlying amyloid pathology, the investigators further investigated those OCT and OCTA parameters in each subgroup with positive or negative amyloid biomarker.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 5
| Arm | Type | Receives |
|---|---|---|
| Dementia | – | –Patients with Alzheimer disease dementia (ADD) fulfilled the NIA-AA core clinical criteria for probable ADD and Aβ positive according to ATN classification scheme. Aβ positive refers to Aβ pathology (CSF Aβ1-42 < 631.8 pg/ml or positive amyloid deposits on 18F-flutemetamol PET by visual inspection). |
| MCI (Mild cognitive impairment) | – | –Patients with mild cognitive impairment (MCI) met the Petersen's criteria. |
| CU (Cognitively unimpaired control) | – | –CU consisted of cognitively unimpaired subjects whose cognition (as defined by the Seoul Neuropsychological Screening Battery (SNSB)) was within normal limits. |
| Aβ positive | – | –Aβ positive refers to Aβ pathology (CSF Aβ1-42 < 631.8 pg/ml or positive amyloid deposits on 18F-flutemetamol PET by visual inspection). |
| Aβ negative | – | –Aβ negative was within normal limits. |
Who may qualify
- Ages
- 50 to 90 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Neurologic Clinic of Pusan National University Hospital
Key inclusion criteria (1 listed)
- Clinical and pathologic diagnosis of ADD or MCI as well as cognitively unimpaired control (CU) from the Neurologic Clinic of Pusan National University Hospital
Key exclusion criteria (9 listed)
- Patient not within the ages of 50-90 years old
- Patient with glaucoma, macular degeneration, retinal vascular disease including diabetic retinopathy, retinal vein occlusion
- Intraocular pressure (IOP) ≥ 21 mmHg
- Dense corneal or ocular media opacity
- History of ocular trauma or associated ocular disease
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
SD-OCT imaging
Time frame: Through study completion, measured at enrollment and analyzed from September 2019 to July 2021
Measuring macular GC/IPLT (μm) and cimcumpapillary RNFLT (μm). The average, minimum, and 6 sectoral (superotemporal, superior, superonasal, inferonasal, inferior, and inferotemporal) GC/IPLT (μm) values are obtained. The average, 4 sectoral (temporal, superior, nasal, and inferior), and 12 clock-hour circumpapillary RNFLT (μm) are obtained. Multiple measurements will not be aggregated, but analyzed respectively.
SD-OCTA imaging
Time frame: Through study completion, measured at enrollment and analyzed from September 2019 to July 2021
Acquiring microvasculature images of macular (6 × 6 mm^2 scan) and optic disc areas (4.5 × 4.5 mm^2 scan). The average vessel density (VD, mm/mm^2) and perfusion density (PD, %) were automatically measured in the Early Treatment of Diabetic Retinopathy Study (ETDRS) grid with values shown in the nine subfields, central, inner, outer and full region. The software calculated the area (mm^2), perimeter (mm), and circularity (defined as 4πA/P^2, where A was the area and P was the perimeter) of foveal avascular zone (FAZ). A circularity closer to 0 means an irregular shape, and closure to 1 indicates a circular shape. Multiple measurements will not be aggregated, but analyzed respectively.
2 secondary outcomes
Diagnostic performance
Time frame: Through study completion, analyzed from July 2021 to July 2022
Correlations
Time frame: Through study completion, analyzed from July 2021 to July 2022
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 26 Jul 2022.
- Background: PubMed 31638686Arvanitakis Z, Shah RC, Bennett DA. Diagnosis and Management of Dementia: Review. JAMA. 2019 Oct 22;322(16):1589-1599. doi: 10.1001/jama.2019.4782.
- Background: PubMed 23477989Villemagne VL, Burnham S, Bourgeat P, Brown B, Ellis KA, Salvado O, Szoeke C, Macaulay SL, Martins R, Maruff P, Ames D, Rowe CC, Masters CL; Australian Imaging Biomarkers and Lifestyle (AIBL) Research Group. Amyloid beta deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study. Lancet Neurol. 2013 Apr;12(4):357-67. doi: 10.1016/S1474-4422(13)70044-9. Epub 2013 Mar 8.
- Background: PubMed 22749065Clark CM, Pontecorvo MJ, Beach TG, Bedell BJ, Coleman RE, Doraiswamy PM, Fleisher AS, Reiman EM, Sabbagh MN, Sadowsky CH, Schneider JA, Arora A, Carpenter AP, Flitter ML, Joshi AD, Krautkramer MJ, Lu M, Mintun MA, Skovronsky DM; AV-45-A16 Study Group. Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-beta plaques: a prospective cohort study. Lancet Neurol. 2012 Aug;11(8):669-78. doi: 10.1016/S1474-4422(12)70142-4. Epub 2012 Jun 28.
- Background: PubMed 21514249Albert MS, DeKosky ST, Dickson D, Dubois B, Feldman HH, Fox NC, Gamst A, Holtzman DM, Jagust WJ, Petersen RC, Snyder PJ, Carrillo MC, Thies B, Phelps CH. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-9. doi: 10.1016/j.jalz.2011.03.008. Epub 2011 Apr 21.
- Background: PubMed 21124753Grossman I, Lutz MW, Crenshaw DG, Saunders AM, Burns DK, Roses AD. Alzheimer's disease: diagnostics, prognostics and the road to prevention. EPMA J. 2010 Jun;1(2):293-303. doi: 10.1007/s13167-010-0024-3. Epub 2010 Jun 29.
- Background: PubMed 20182034Kirby E, Bandelow S, Hogervorst E. Visual impairment in Alzheimer's disease: a critical review. J Alzheimers Dis. 2010;21(1):15-34. doi: 10.3233/JAD-2010-080785.
- Background: PubMed 17071920Hodges JR. Alzheimer's centennial legacy: origins, landmarks and the current status of knowledge concerning cognitive aspects. Brain. 2006 Nov;129(Pt 11):2811-22. doi: 10.1093/brain/awl275.
- Background: PubMed 1996878Cronin-Golomb A, Corkin S, Rizzo JF, Cohen J, Growdon JH, Banks KS. Visual dysfunction in Alzheimer's disease: relation to normal aging. Ann Neurol. 1991 Jan;29(1):41-52. doi: 10.1002/ana.410290110.
- Background: PubMed 2819446Blanks JC, Hinton DR, Sadun AA, Miller CA. Retinal ganglion cell degeneration in Alzheimer's disease. Brain Res. 1989 Nov 6;501(2):364-72. doi: 10.1016/0006-8993(89)90653-7.
- Background: PubMed 2314849Sadun AA, Bassi CJ. Optic nerve damage in Alzheimer's disease. Ophthalmology. 1990 Jan;97(1):9-17. doi: 10.1016/s0161-6420(90)32621-0.
- Background: PubMed 29394263Jiang H, Liu Y, Wei Y, Shi Y, Wright CB, Sun X, Rundek T, Baumel BS, Landman J, Wang J. Impaired retinal microcirculation in patients with Alzheimer's disease. PLoS One. 2018 Feb 2;13(2):e0192154. doi: 10.1371/journal.pone.0192154. eCollection 2018.
- Background: PubMed 20946471Brown WR, Thore CR. Review: cerebral microvascular pathology in ageing and neurodegeneration. Neuropathol Appl Neurobiol. 2011 Feb;37(1):56-74. doi: 10.1111/j.1365-2990.2010.01139.x.
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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.
Eun-Joo Kim, MD, PhD principal investigator
Department of Neurology, Pusan National University Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Alzheimer Disease and Amyloid Angiopathy, run by Pusan National University Hospital at 1 site in South Korea.
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 1 inclusion and 9 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: finished, as of the sponsor's last update on 26 Jul 2022. 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 South Korea. 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. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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?
SD-OCT imaging (time frame: Through study completion, measured at enrollment and analyzed from September 2019 to July 2021). The study lists 2 primary outcomes in all. 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 NCT05475158, which also lists 24 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 26 Jul 2022.