Abstract
Purpose
These guidelines aim to support magnetic resonance imaging (MRI) diagnosis in patients receiving anti-amyloid β (Aβ) antibody treatment without restricting treatment eligibility.
Materials and methods
These guidelines were collaboratively established by Japan Radiological Society, The Japanese Society of Neuroradiology, and Japanese Society for Magnetic Resonance in Medicine by reviewing existing literature and the results of clinical trials.
Results
Facility standards should comply with the “Optimal Use Promotion Guidelines” of Japan, and physicians should possess comprehensive knowledge of amyloid-related imaging abnormalities (ARIA) and expertise in brain MRI interpretation. The acquisition of knowledge regarding amyloid-related imaging abnormalities, brain MRI, anti-Aβ antibody introduction, and post-treatment diagnosis are also recommended.
Conclusion
These guidelines facilitate the accurate diagnosis and effective management of ARIA; ensure the safe administration of anti-Aβ drugs; and provide a framework for MRI facilities, includes staffing requirements and the use of MRI management systems.
Supplementary Information
The online version contains supplementary material available at 10.1007/s11604-025-01773-x.
Keywords: Guidelines, Brain, Magnetic resonance imaging, Anti-amyloid beta antibody treatment, Alzheimer's disease, Amyloid-related imaging abnormalities
Introduction
For the treatment of early Alzheimer’s disease (AD), the Food and Drug Administration approved anti-amyloid β (Aβ) monoclonal antibodies: lecanemab (LeqembiTM) on July 6, 2023, and donanemab (Kisunla) on July 2, 2024. In Japan, lecanemab was approved by the Japanese regulatory authorities on September 25, 2023, and was covered by the Japanese health insurance on December 20 [1]. More recently, in Japan, medication coverage for donanemab became available on November 24, 2024. Randomized clinical trials have shown that the use of anti-Aβ antibodies is associated with magnetic resonance imaging (MRI) signal abnormalities treatment-related adverse events called amyloid-related imaging abnormalities (ARIA) [2–11]. Given that the presence of any hemorrhage on initial MRI (anti-Aβ antibody introduction MRI) increases the risk of ARIA [12], the detection of cerebral microbleeds and superficial hemosiderosis on initial MRI is crucial. During drug treatment, ARIA detection and severity assessment are vital for determining whether to continue, suspend, discontinue, or resume therapy. Consequently, brain MRI plays a vital role in patients considered for anti-Aβ antibody treatment. The roles of MRI include the following: (1) assessment of eligibility for therapy, including differential diagnosis of dementia for initial MRI, and (2) detection and diagnosis of ARIA for follow-up (on- or post-treatment) MRI. Diagnostic imaging physicians are required to possess comprehensive knowledge of ARIA and general skills in interpreting brain MRI findings, including cerebrovascular diseases, brain tumors, inflammatory conditions, traumatic brain injuries, metabolic diseases, and malformations. Although Japan has the highest MRI accessibility worldwide, there are relatively few radiologists specializing in neuroradiology who can detect subtle abnormalities [13].
Prompt diagnosis and management of ARIA are essential for the safe administration of anti-Aβ drugs. ARIA is often characterized by subtle abnormalities, emphasizing the need for quality control of MRI. Considering that patients with ARIA may require urgent attention, an institutional framework for MRI facilities is essential. This framework includes staffing requirements, such as diagnostic imaging physicians and radiological technologists, as well as an MRI management system that can maintain appropriate imaging protocols. Although there are reviews and guidelines on the radiological, biological, and clinical characteristics of ARIA [12, 14], a few reviews discuss the differential diagnosis of dementia and ARIA on initial MRI in treated patients. Furthermore, there are no practical guidelines addressing facility requirements, qualifications for diagnostic imaging physicians, and required knowledge. Therefore, Japan Radiological Society (https://www.radiology.jp/english/index.html), The Japanese Society of Neuroradiology (https://neurorad.jp/english-page/), and Japanese Society for Magnetic Resonance in Medicine (https://www.jsmrm.jp/modules/en/index.php?content_id=1) collaboratively present these guidelines for brain MRI examination and MRI-based diagnosis in patients undergoing anti-Aβ antibody treatment.
Framework for MRI diagnosis
Institutional requirements
Facility standards should comply with the “Optimal Use Promotion Guidelines,” which are national regulations in Japan aimed at ensuring the appropriate use of medical imaging resources. MRI facilities should strive to maintain management systems equivalent to Added fees for Radiological Managements on Imaging-studies (ARMIs) 3 or 4, with full-time radiologists*. A collaborative system between prescribing physicians and brain MRI diagnosticians is essential, and efforts should be made to conduct examinations using protocols that are standardized across the same MRI equipment whenever possible.
Diagnostic imaging physician qualifications
Diagnostic imaging physicians should possess expertise in brain MRI interpretation, encompassing not only dementia-related findings but also cerebrovascular lesions, brain tumors, inflammatory diseases, traumatic injuries, metabolic conditions, and congenital anomalies.
Diagnostic imaging physicians should explain the importance and necessity of appropriate protocols to radiological technologists (primarily referring to Magnetic Resonance Technological Specialists**) and optimize ARIA imaging protocols with radiological technologists at each facility. Diagnostic imaging physicians should establish STAT reporting systems*** for urgent MRI interpretation in accordance with guidelines from relevant societies (The Japan Radiological Society and The Japanese College of Radiology) and maintain collaboration with radiological technologists for emergency findings.
To ensure continuity of MRI examinations, consideration should be given to conducting MRI examinations at affiliated facilities when both the quality of examinations and diagnostic imaging are assured, similar to amyloid positron emission tomography (PET) or cerebrospinal fluid (CSF) examinations.
Knowledge requirements for diagnostic imaging physicians
Variations in MRI equipment among vendors, magnetic field strength, and MRI sequences influence the image findings of ARIA. Therefore, the three MRI-related academic societies (The Japan Radiological Society, The Japanese Society for Neuroradiology, and The Japanese Society for Magnetic Resonance in Medicine) propose acquiring the following knowledge:
About ARIA [5, 8, 12, 14–16]
Classification (ARIA-E and ARIA-H)
Pathophysiology (incidence, clinical presentation, timing, and progression)
Diagnostic criteria, severity classification, and management strategies.
Brain MRI
Although protocols are not fully established, Table 1 shows the recommended protocol by the three societies based on phase III clinical trials. Baseline and follow-up MRI should use identical imaging parameters on the same equipment. For brain MRI diagnosis, knowledge of the following imaging sequences is recommended:
Differences between 3 and 2D imaging (T1 weighted imaging, fluid-attenuated inversion recovery [FLAIR], etc.) [17]
Basic knowledge of T2* gradient-echo (GRE) sequence and susceptibility-weighted imaging (SWI) sequence [18]
Knowledge of imaging protocol parameters (e.g., repetition time [TR], echo time [TE], and inversion time [TI]) and their impact on image visualizations
Impact on image visualization by MRI equipment variations among vendors, and relationship between field strength and image visualizations (1.5 T vs. 3 T equipment)
Relationship between imaging parameters (TR, TE, and TI) and image visualizations (e.g., FLAIR) [17, 19], relationship between slice thickness and lesion detection [20]
Knowledge regarding diffusion-weighted imaging (DWI) and apparent diffusion coefficient map [12]
Relationship between parallel imaging and acquisition time/image quality [21, 22]
Knowledge of vendor-specific imaging methods, their sequence names, visualization capabilities, and artifacts (particularly for SWI, similar sequences include the Principle of Echo Shifting with a Train of Observation and T2 Star Weighted magnetic resonance Angiography)
Knowledge of brain volume analysis (voxel-based morphometry [23–26]), advanced imaging techniques (e.g., compressed sensing [27], AI-based noise reduction [28, 29]), and pathophysiological analysis using brain MRI (e.g., diffusion tensor imaging, diffusion tensor image analysis along the perivascular space: Diffusion Tensor Imaging–Analysis Along the Perivascular Space method) [30, 31].
Table 1.
MRI sequences to be included in the imaging protocol (as recommended by three societiesa)
| MRI sequences | Purpose | Initial (baseline) | Follow-up (asymptomatic) | Follow-up (symptomatic) |
|---|---|---|---|---|
| 3D-T1WI | Brain volume evaluation (atrophy) | 〇 | △ | △ |
| DWI | Differential diagnosis of acute cerebral infarction | ◎ | ◎ | ◎ |
| T2WI | Detection of various lesions | 〇 | 〇 | |
| FLAIR | Diagnosis of ARIA-E | ◎ | ◎ | ◎ |
| T2* GRE or SWIb | Diagnosis of ARIA-H | ◎ | ◎ | ◎ |
| T2WI (Cor) | Evaluation of hippocampal atrophy | 〇 | ||
| MR angiography | Evaluation of vascular lesions (stenosis and aneurysms) | 〇 | 〇 | |
| Gd-T1WIc | Detection of enhanced brain lesions (metastases, meningitis, etc.) | △ |
DWI diffusion-weighted imaging, FLAIR fluid-attenuated inversion recovery, GRE gradient-echo, SWI susceptibility-weighted imaging
◎ = essential MRI sequence, 〇 = recommended MRI sequence, △ = optional MRI sequence, blank field: omissible MRI sequence
aJapan Radiological Society, The Japanese Society for Neuroradiology, and Japanese Society for Magnetic Resonance in Medicine
bFor ARIA-H evaluation, SWI can also be used instead of T2* GRE. Although SWI has higher sensitivity for detecting cerebral microbleeds compared to T2* GRE, SWI-capable equipment may be limited
cAdditional examinations with gadolinium contrast may be performed when further lesion differentiation is needed
Initial MRI (anti-Aβ antibody introduction) diagnosis (Table 2)
Table 2.
Diseases and conditions included in the initial (drug introduction) MRI diagnosis
| Diseases and conditions suggesting non-AD dementia with clinical significance | Diseases and conditions impacting treatment efficacy with significant role of diagnostic imaging |
|---|---|
| Degenerative dementia | Amyloid angiopathy-related inflammationa |
| Alzheimer’s disease | Vascular lesions (cerebral aneurysm, arteriovenous fistula) |
| Lewy body disease, dementia with Parkinson's | Idiopathic normal pressure hydrocephalus (adult chronic hydrocephalus Hakim's disease) |
| Argyrophilic grain disease | Vascular malformations: cavernous hemangioma, arteriovenous malformation, venous malformation |
| Frontotemporal lobar degeneration (FTLD) | Brain tumorsb |
| Progressive supranuclear palsy (PSP) | PML |
| Corticobasal degeneration (CBD) | Neurosyphilis |
| Senile dementia of the neurofibrillary tangle (SD-NFT) | Epilepsy |
| Globular glial tauopathy (GGT) | Alcohol-related |
| Chronic traumatic encephalopathy | Post-seizure encephalopathy |
| AIDS-related encephalopathy | |
| Vascular dementia | Neuroinfection |
| Large territory infarction, hemorrhage | Vasculitis |
| Binswanger’s disease | Demyelinating diseases |
| Strategic infarct dementia | Toxicity: carbon monoxide poisoning, drugs, metals |
| Cortical microinfarcts | Prion disease |
| Cerebral amyloid angiopathy | Neuronal intranuclear inclusion disease |
| Hypoperfusion | ALSP/HDLS-CSF1R |
| Chronic subdural hematoma | White matter diseases (various pathologies) |
| Traumatic brain injury (TBI) | |
| Brain contusion, diffuse axonal injury, chronic subdural hematoma, chronic traumatic encephalopathy (CTE) | |
| Nutritional/metabolic disorders: vitamin B1 deficiency, vitamin B12 deficiency, folate deficiency, etc | |
| Organ failure and related diseases: hepatic encephalopathy, renal failure |
PML progressive multifocal leukoencephalopathy, AIDS acquired immune deficiency syndrome, ALSP adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, HDLS-CSF1R hereditary diffuse leukoencephalopathy with spheroid due to CSF1R mutations
aConsidered to have similar pathology to ARIA
bMeningiomas or arachnoid cysts diagnosed as lesions with maximum diameters < 1 cm are not excluded for drug administration
Assessment should be made regarding contraindications for anti-Aβ antibody introduction (check Sheet A in Supplementary material). In addition to diagnosing ARIA (spontaneous ARIA), diagnostic imaging physicians must perform standard brain MRI diagnosis. Therefore, knowledge of MRI findings [32, 33] for AD and non-AD conditions affecting cognitive function is required. The cognitive dysfunction-presenting non-AD degenerative diseases include Lewy body dementia [34, 35], frontotemporal lobar degeneration [36], argyrophilic grain disease, corticobasal degeneration [37], cerebral infarction/hemorrhage [38, 39], subdural hematoma, encephalitis/encephalopathy, traumatic brain injury (TBI) (brain contusion, diffuse axonal injury [DAI]) [40, 41], idiopathic normal pressure hydrocephalus (adult chronic hydrocephalus Hakim’s disease) [42], brain tumors (hemorrhagic metastases), vascular malformations/hemangiomas (cavernous hemangioma), vascular lesions (cerebral aneurysms, arteriovenous malformation/fistulas), inflammatory diseases (infection, autoimmune encephalopathy), cerebral amyloid angiopathy (CAA) [43, 44], neuronal intranuclear inclusion disease [45], and others.
Follow-up MRI (on- or post-treatment) diagnosis
Refer to Check Sheet B (Supplementary material) created by the three societies for ARIA-E and ARIA-H detection and severity assessment. Before MRI interpretation, diagnostic imaging physicians should confirm whether the imaging equipment and conditions match the initial MRI, including TR, TE, TI, and spatial resolution parameters. MRI diagnosis includes regular follow-up, follow-up for patients with ARIA, and emergency MRI for symptomatic cases. Regular follow-up includes initial MRI diagnosis plus ARIA-E and ARIA-H detection and severity assessment (number, extent, and size of lesions, if detected). For patients with ARIA, follow-up includes the evaluation of ARIA changes. Emergency MRI requires sequence selection (potentially including contrast) and differential diagnosis based on symptoms (Tables 2, 3, 4).
Table 3.
Differential diagnoses of ARIA-E, pathologies/diseases, and MRI findings
| ARIA-E (brain parenchymal edema) and similar findings | ARIA-E (sulcal effusion) and similar findings |
|---|---|
| MR sequence related/anatomical causes | MR sequence related/anatomical causes |
| Signal changes due to imaging parameter settings | Water signal suppression failure |
| Susceptibility artifacts (mostly iatrogenic): | |
| Pathologies/diseases | Metal (dental work, clips, coils), oxygen administration, recent Gd contrast administration, increased blood pool ratio |
| Acute cerebral infarction (arterial, venous) | |
| Brain tumors (metastatic, primary), bloomy rind sign | Motion Artifacts |
| Traumatic brain injury (TBI) | CSF inflow, vascular pulsation, body movement |
| Brain edema from extra-axial masses | |
| Infectious encephalitis, metabolic encephalopathy | Pathologies/Diseases |
| Autoimmune encephalitis/encephalopathy | Accumulation |
| Epilepsy, familial hemiplegic migraine | Subarachnoid hemorrhage, fat components, amyloid |
| Progressive multifocal leukoencephalopathy (PML) | Infiltration: |
| Posterior reversible encephalopathy syndrome (PRES) | Meningeal carcinomatosis, melanomatosis, sarcoidosis |
| Flow | |
| Intravascular signals (embolism, ivy sign, hyperperfusion) | |
| Meningitis and its sequelae |
Table 4.
Differential diagnoses of ARIA-H, pathologies/diseases, and MRI findings
| ARIA-H (cerebral microbleeds, hemorrhage) | ARIA-H (superficial hemosiderosis) |
|---|---|
| MR sequence related/anatomical causes | MR sequence related/anatomical causes |
| Normal vessels (vascular signal void) | Skull base susceptibility artifacts |
| Physiological calcification | |
| Pathologies/Diseases | |
| Pathologies/Diseases | Subarachnoid hemorrhage |
| Conditions with calcification | Trauma |
| Cavernous hemangioma/vascular malformation | Cerebral aneurysm, arteriovenous malformation |
| Hypertensive microbleeds and cerebral amyloid angiopathy | Cerebral venous thrombosis |
| Embolic microbleeds: fat, air, IE, sepsis, HbS disease, ITP | RCVS |
| Traumatic brain injury (TBI): | Remote cerebellar hemorrhage |
| Diffuse axonal injury (DAI), cerebral small vessel injury | Vasculitis |
| Brain contusion | Spinal duropathy |
| Brain tumors | Pseudo laminar cortical necrosis |
| Hemorrhagic metastases: melanoma, renal, thyroid, lung, myxoma | Post-infarct cortical hemorrhagic transformation |
| Vasculitis | Subdural hematoma-related |
| PCNSV, secondary: infection, tumor, drug-related | |
| Post-radiation | |
| Hereditary | |
| CADASIL/CARASIL, COL4A1-related diseases, Fabry disease |
HbS sickle cell disease, IE infective endocarditis, ITP idiopathic thrombocytopenic purpura, CADASIL cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, CARASIL cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy, PCNSV primary central nervous system vasculitis, RCVS, reversible cerebral vasoconstriction syndrome
Knowledge required for ARIA-E assessment (Table 3)
FLAIR sequence–related/anatomical causes [46]: false positives due to water signal suppression failure, artifacts from air, bone (skull base), foreign objects (metals etc.), oxygen administration, increased blood pool ratio, recent Gd contrast administration, and motion artifacts (CSF inflow, vascular pulsation, body movement)
Differentiation between vasogenic and cytotoxic edema on DWI [47]
ARIA-E (edema) differential diagnoses [11, 48, 49]: acute cerebral infarction, posterior reversible encephalopathy syndrome, progressive multifocal leukoencephalopathy, encephalitis/encephalopathy (infectious, non-infectious, metabolic, autoimmune), brain tumors (primary brain tumors, edema due to extra-axial masses, metastatic brain tumors), TBI, and epilepsy-related brain changes
ARIA-E (effusion) differential diagnoses [11, 48, 49]: subarachnoid hemorrhage, meningitis and its sequelae, high signal in sulci associated with cerebral artery occlusion (ivy sign).
Knowledge required for ARIA-H assessment (Table 4)
T2*GRE and SWI sequence related/Anatomical causes [50]: normal vessels (vascular signal void), physiological calcification, susceptibility artifacts (e.g., skull base)
Diagnosis of microbleeds, superficial hemosiderosis, and cerebral hemorrhage. In the diagnosis of microbleeds, although the cause (hypertensive or CAA) is clinically important, the anatomical location (etiology of microbleeds) is not considered in the severity classification of ARIA-H.
ARIA-H (intracerebral hemorrhage) differential diagnoses [51]: cavernous hemangioma/vascular malformation, TBI (brain contusion, DAI)
ARIA-H (superficial hemosiderosis) differential diagnoses [52]: subarachnoid hemorrhage, post-traumatic changes, and subdural hematoma and its history [53].
Final notes
These guidelines aim to support MRI diagnosis in patients receiving anti-Aβ antibody treatment without restricting treatment eligibility. Although current guidelines address the latest approved drugs, the basic principles will apply to new medications, with updates planned as new information becomes available. Therefore, regular updates are necessary for aspects outside these guidelines, including amyloid PET examination and ARIA management.
Annotations
* ARMIs: A supplementary payment system in the Japanese medical insurance system to ensure quality of diagnostic imaging. The system has four tiers (1–4) based on facility implementation and management systems. One of the requirements for ARMIs 3 and 4 is the presence of three or more and six or more full-time diagnostic imaging physicians, respectively.
** Magnetic Resonance Technological Specialist: A technologist in Japan certified by the Japan Authorize Organization for Magnetic Resonance Technological Specialist who works with magnetic resonance examinations, with the purpose of ensuring international equivalency of magnetic resonance examination techniques, providing standardized optimal imaging information that accommodates the latest medical technologies, and guaranteeing safety.
*** STAT Image Reporting: Refers to the act of radiological technologists providing findings of STAT images to physicians according to the “Guidelines for Reporting STAT Image Findings of High-Emergency Diseases Affecting Life Prognosis” by the Japan Radiological Society and the Japanese Society of Radiological Technology. STAT images refer to “images showing findings of high-emergency diseases affecting life prognosis,” derived from the Latin word “statim,” which directly translates to “immediately.”
Supplementary Information
Below is the link to the electronic supplementary material.
Funding
None.
Declarations
Conflict of interest
None.
Ethical statement
Not applicable.
Footnotes
This article has been jointly published in Magnetic Resonance in Medical Sciences.
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Iwatsubo T. Development of disease-modifying therapies against Alzheimer’s disease. Psychiatry Clin Neurosci. 2024;78:491–4. 10.1111/pcn.13681. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Karran E, De Strooper B. The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics. Nat Rev Drug Discov. 2022;21:306–18. 10.1038/s41573-022-00391-w. [DOI] [PubMed] [Google Scholar]
- 3.Hampel H, Cummings J, Blennow K, Gao P, Jack CR, Vergallo A. Developing the ATX(N) classification for use across the Alzheimer disease continuum. Nat Rev Neurol. 2021;17:580–9. 10.1038/s41582-021-00520-w. [DOI] [PubMed] [Google Scholar]
- 4.van Dyck CH, Swanson CJ, Aisen P, Bateman RJ, Chen C, Gee M, et al. Lecanemab in early Alzheimer’s disease. N Engl J Med. 2023;388:9–21. 10.1056/NEJMoa2212948. [DOI] [PubMed] [Google Scholar]
- 5.Salloway S, Chalkias S, Barkhof F, Burkett P, Barakos J, Purcell D, et al. Amyloid-related imaging abnormalities in 2 phase 3 studies evaluating aducanumab in patients with early Alzheimer disease. JAMA Neurol. 2022;79:13–21. 10.1001/jamaneurol.2021.4161. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Sperling R, Salloway S, Brooks DJ, Tampieri D, Barakos J, Fox NC, et al. Amyloid-related imaging abnormalities in patients with Alzheimer’s disease treated with Bapineuzumab: a retrospective analysis. Lancet Neurol. 2012;11:241–9. 10.1016/S1474-4422(12)70015-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Carlson C, Siemers E, Hake A, Case M, Hayduk R, Suhy J, et al. Amyloid-related imaging abnormalities from trials of solanezumab for Alzheimer’s disease. Alzheimers Dement (Amst). 2016;2:75–85. 10.1016/j.dadm.2016.02.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Ketter N, Brashear HR, Bogert J, Di J, Miaux Y, Gass A, et al. Central review of amyloid-related imaging abnormalities in two phase III clinical trials of Bapineuzumab in mild-to-moderate Alzheimer’s disease patients. J Alzheimers Dis. 2017;57:557–73. 10.3233/JAD-160216. [DOI] [PubMed] [Google Scholar]
- 9.Barakos J, Purcell D, Suhy J, Chalkias S, Burkett P, Marsica Grassi C, et al. Detection and management of amyloid-related imaging abnormalities in patients with Alzheimer’s disease treated with anti-amyloid beta therapy. J Prev Alzheimers Dis. 2022;9:211–20. 10.14283/jpad.2022.21. [DOI] [PubMed] [Google Scholar]
- 10.Sperling RA, Jack CR, Black SE, Frosch MP, Greenberg SM, Hyman BT, et al. Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: recommendations from the Alzheimer’s Association research roundtable workgroup. Alzheimers Dement. 2011;7:367–85. 10.1016/j.jalz.2011.05.2351. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Barakos J, Sperling R, Salloway S, Jack C, Gass A, Fiebach JB, et al. MR imaging features of amyloid-related imaging abnormalities. AJNR Am J Neuroradiol. 2013;34:1958–65. 10.3174/ajnr.A3500. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Cogswell PM, Barakos JA, Barkhof F, Benzinger TS, Jack CR, Poussaint TY, et al. Amyloid-related imaging abnormalities with emerging Alzheimer disease therapeutics: detection and reporting recommendations for clinical practice. AJNR Am J Neuroradiol. 2022;43:E19–35. 10.3174/ajnr.A7586. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Kumamaru KK, Machitori A, Koba R, Ijichi S, Nakajima Y, Aoki S. Global and Japanese regional variations in radiologist potential workload for computed tomography and magnetic resonance imaging examinations. Jpn J Radiol. 2018;36:273–81. 10.1007/s11604-018-0724-5. [DOI] [PubMed] [Google Scholar]
- 14.Hampel H, Elhage A, Cho M, Apostolova LG, Nicoll JAR, Atri A. Amyloid-related imaging abnormalities (ARIA): radiological, biological and clinical characteristics. Brain. 2023;146:4414–24. 10.1093/brain/awad188. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Greenberg SM, Bacskai BJ, Hernandez-Guillamon M, Pruzin J, Sperling R, van Veluw SJ. Cerebral amyloid angiopathy and Alzheimer disease: one peptide, two pathways. Nat Rev Neurol. 2020;16:30–42. 10.1038/s41582-019-0281-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Filippi M, Cecchetti G, Spinelli EG, Vezzulli P, Falini A, Agosta F. Amyloid-related imaging abnormalities and β-amyloid-targeting antibodies: a systematic review. JAMA Neurol. 2022;79:291–304. 10.1001/jamaneurol.2021.5205. [DOI] [PubMed] [Google Scholar]
- 17.Kakeda S, Korogi Y, Hiai Y, Ohnari N, Sato T, Hirai T. Pitfalls of 3D FLAIR brain imaging: a prospective comparison with 2D FLAIR. Acad Radiol. 2012;19:1225–32. 10.1016/j.acra.2012.04.017. [DOI] [PubMed] [Google Scholar]
- 18.Tong KA, Ashwal S, Holshouser BA, Shutter LA, Herigault G, Haacke EM, et al. Hemorrhagic shearing lesions in children and adolescents with posttraumatic diffuse axonal injury: improved detection and initial results. Radiology. 2003;227:332–9. 10.1148/radiol.2272020176. [DOI] [PubMed] [Google Scholar]
- 19.Okuda T, Korogi Y, Shigematsu Y, Sugahara T, Hirai T, Ikushima I, et al. Brain lesions: when should fluid-attenuated inversion-recovery sequences be used in MR evaluation? Radiology. 1999;212:793–8. 10.1148/radiology.212.3.r99se07793. [DOI] [PubMed] [Google Scholar]
- 20.Hayashida Y, Kakeda S, Hiai Y, Ide S, Ogasawara A, Ooki H, et al. Diagnosis of intracranial hemorrhagic lesions: comparison between 3D-SWAN (3D T2*-weighted imaging with multi-echo acquisition) and 2D–T2*-weighted imaging. Acta Radiol. 2014;55:201–7. 10.1177/0284185113495836. [DOI] [PubMed] [Google Scholar]
- 21.Hiai Y, Kakeda S, Sato T, Ohnari N, Moriya J, Kitajima M, et al. 3D TOF MRA of intracranial aneurysms at 1.5 T and 3 T: influence of matrix, parallel imaging, and acquisition time on image quality: a vascular phantom study. Acad Radiol. 2008;15:635–40. 10.1016/j.acra.2007.12.021. [DOI] [PubMed] [Google Scholar]
- 22.Goncalves Filho ALM, Awan KM, Conklin J, Ngamsombat C, Cauley SF, Setsompop K, et al. Validation of a highly accelerated post-contrast wave-controlled aliasing in parallel imaging (CAIPI) 3D–T1 MPRage compared to standard 3D–T1 MPRage for detection of intracranial enhancing lesions on 3-T MRI. Eur Radiol. 2023;33:2905–15. 10.1007/s00330-022-09265-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Schultz V, Hedderich DM, Schmitz-Koep B, Schinz D, Zimmer C, Yakushev I, et al. Removing outliers from the normative database improves regional atrophy detection in single-subject voxel-based morphometry. Neuroradiology. 2024;66:507–19. 10.1007/s00234-024-03304-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Inui S, Kaneda D, Sakurai K, Uchida Y, Abe O, Hashizume Y. Voxel-based morphometry of Alzheimer’s disease using a localizer image: a comparative study with magnetization prepared rapid acquisition with gradient echo. Magn Reson Med Sci. 2025;24:103–11. 10.2463/mrms.mp.2023-0093. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Goto M, Kamagata K, Andica C, Takabayashi K, Uchida W, Goto T, et al. Deep learning-based hierarchical brain segmentation with preliminary analysis of the repeatability and reproducibility. Magn Reson Med Sci. 2024. 10.2463/mrms.mp.2023-0124. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Das SR, Ilesanmi A, Wolk DA, Gee JC. Beyond macrostructure: is there a role for radiomics analysis in neuroimaging? Magn Reson Med Sci. 2024;23:367–76. 10.2463/mrms.rev.2024-0053. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Kim HG, Oh SW, Han D, Kim JY, Lim GY. Accelerated 3D T2-weighted images using compressed sensing for pediatric brain imaging. Neuroradiology. 2022;64:2399–407. 10.1007/s00234-022-03028-2. [DOI] [PubMed] [Google Scholar]
- 28.Iwamura M, Ide S, Sato K, Kakuta A, Tatsuo S, Nozaki A, et al. Thin-slice two-dimensional T2-weighted imaging with deep learning-based reconstruction: improved lesion detection in the brain of patients with multiple sclerosis. Magn Reson Med Sci. 2024;23:184–92. 10.2463/mrms.mp.2022-0112. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Estler A, Hauser TK, Mengel A, Brunnée M, Zerweck L, Richter V, et al. Deep learning accelerated image reconstruction of fluid-attenuated inversion recovery sequence in brain imaging: reduction of acquisition time and improvement of image quality. Acad Radiol. 2024;31:180–6. 10.1016/j.acra.2023.05.010. [DOI] [PubMed] [Google Scholar]
- 30.Saito Y, Kamagata K, Andica C, Uchida W, Takabayashi K, Yoshida S, et al. Reproducibility of automated calculation technique for diffusion tensor image analysis along the perivascular space. Jpn J Radiol. 2023;41:947–54. 10.1007/s11604-023-01415-0. [DOI] [PubMed] [Google Scholar]
- 31.Saito Y, Kamagata K, Andica C, Taoka T, Tuerxun R, Uchida W, et al. Multisite harmonization of diffusion tensor image analysis along the perivascular space using the COMBined association test. Jpn J Radiol. 2023;41:1072–83. 10.1007/s11604-023-01432-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Lai YLL, Hsu FT, Yeh SY, Kuo YT, Lin HH, Lin YC, et al. Atrophy of the cholinergic regions advances from early to late mild cognitive impairment. Neuroradiology. 2024;66:543–56. 10.1007/s00234-024-03290-6. [DOI] [PubMed] [Google Scholar]
- 33.Wittens MMJ, Allemeersch GJ, Sima DM, Vanderhasselt T, Raeymaeckers S, Fransen E, et al. Towards validation in clinical routine: a comparative analysis of visual MTA ratings versus the automated ratio between inferior lateral ventricle and hippocampal volumes in Alzheimer’s disease diagnosis. Neuroradiology. 2024;66:487–506. 10.1007/s00234-024-03280-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium. Neurology. 2017;89:88–100. 10.1212/WNL.0000000000004058. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Sakurai K, Kaneda D, Morimoto S, Uchida Y, Inui S, Shang C, et al. Medial temporal atrophy predicts the limbic comorbidities in lewy body disease. Neuroradiology. 2025;67:65–77. 10.1007/s00234-024-03502-z. [DOI] [PubMed] [Google Scholar]
- 36.Lashley T, Rohrer JD, Mead S, Revesz T. Review: an update on clinical, genetic and pathological aspects of frontotemporal lobar degenerations. Neuropathol Appl Neurobiol. 2015;41:858–81. 10.1111/nan.12250. [DOI] [PubMed] [Google Scholar]
- 37.Sakurai K, Tokumaru AM, Yoshida M, Saito Y, Wakabayashi K, Komori T, et al. Conventional magnetic resonance imaging key features for distinguishing pathologically confirmed corticobasal degeneration from its mimics: a retrospective analysis of the J-VAC study. Neuroradiology. 2024;66:1917–29. 10.1007/s00234-024-03432-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Sachdev P, Kalaria R, O’Brien J, Skoog I, Alladi S, Black SE, et al. Diagnostic criteria for vascular cognitive disorders: a VASCOG statement. Alzheimer Dis Assoc Disord. 2014;28:206–18. 10.1097/WAD.0000000000000034. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Quintas-Neves M, Almeida FC, Gauthreaux K, Teylan MA, Mock CN, Kukull WA, et al. Fazekas scale magnetic resonance imaging assessment in Alzheimer’s disease and primary age-related tauopathy. Neuroradiology. 2024;66:2185–93. 10.1007/s00234-024-03464-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Graham NS, Sharp DJ. Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia. J Neurol Neurosurg Psychiatry. 2019;90:1221–33. 10.1136/jnnp-2017-317557. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Graham NSN, Jolly A, Zimmerman K, Bourke NJ, Scott G, Cole JH, et al. Diffuse axonal injury predicts neurodegeneration after moderate-severe traumatic brain injury. Brain. 2020;143:3685–98. 10.1093/brain/awaa316. [DOI] [PubMed] [Google Scholar]
- 42.Tullberg M, Toma AK, Yamada S, Laurell K, Miyajima M, Watkins LD, et al. Classification of chronic hydrocephalus in adults: a systematic review and analysis. World Neurosurg. 2024;183:113–22. 10.1016/j.wneu.2023.12.094. [DOI] [PubMed] [Google Scholar]
- 43.Charidimou A, Boulouis G, Frosch MP, Baron JC, Pasi M, Albucher JF, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI-neuropathology diagnostic accuracy study. Lancet Neurol. 2022;21:714–25. 10.1016/S1474-4422(22)00208-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44.Sakurai K, Tokumaru AM, Nakatsuka T, Murayama S, Hasebe S, Imabayashi E, et al. Imaging spectrum of sporadic cerebral amyloid angiopathy: multifaceted features of a single pathological condition. Insights Imaging. 2014;5:375–85. 10.1007/s13244-014-0312-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Sone J, Kitagawa N, Sugawara E, Iguchi M, Nakamura R, Koike H, et al. Neuronal intranuclear inclusion disease cases with leukoencephalopathy diagnosed via skin biopsy. J Neurol Neurosurg Psychiatry. 2014;85:354–6. 10.1136/jnnp-2013-306084. [DOI] [PubMed] [Google Scholar]
- 46.Stuckey SL, Goh TD, Heffernan T, Rowan D. Hyperintensity in the subarachnoid space on FLAIR MRI. AJR Am J Roentgenol. 2007;189:913–21. 10.2214/AJR.07.2424. [DOI] [PubMed] [Google Scholar]
- 47.Le Bihan D, Turner R, Douek P, Patronas N. Diffusion MR imaging: clinical applications. AJR Am J Roentgenol. 1992;159:591–9. 10.2214/ajr.159.3.1503032. [DOI] [PubMed] [Google Scholar]
- 48.Roytman M, Mashriqi F, Al-Tawil K, Schulz PE, Zaharchuk G, Benzinger TLS, et al. Amyloid-related imaging abnormalities: an update. AJR Am J Roentgenol. 2023;220:562–74. 10.2214/AJR.22.28461. [DOI] [PubMed] [Google Scholar]
- 49.Agarwal A, Gupta V, Brahmbhatt P, Desai A, Vibhute P, Joseph-Mathurin N, et al. Amyloid-related imaging abnormalities in Alzheimer disease treated with anti-amyloid-β therapy. Radiographics. 2023;43: e230009. 10.1148/rg.230009. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50.Haller S, Haacke EM, Thurnher MM, Barkhof F. Susceptibility-weighted imaging: technical essentials and clinical neurologic applications. Radiology. 2021;299:3–26. 10.1148/radiol.2021203071. [DOI] [PubMed] [Google Scholar]
- 51.Tsushima Y, Endo K. Hypointensities in the brain on T2*-weighted gradient-echo magnetic resonance imaging. Curr Probl Diagn Radiol. 2006;35:140–50. 10.1067/j.cpradiol.2006.04.002. [DOI] [PubMed] [Google Scholar]
- 52.Weidauer S, Neuhaus E, Hattingen E. Cerebral superficial siderosis: etiology, neuroradiological features and clinical findings. Clin Neuroradiol. 2023;33:293–306. 10.1007/s00062-022-01231-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 53.Kakeda S, Korogi Y, Ohnari N, Nishimura J, Moriya J, Yamamoto J, et al. Superficial siderosis associated with a chronic subdural hematoma: T2-weighted MR imaging at 3T. Acad Radiol. 2010;17:871–6. 10.1016/j.acra.2010.02.014. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.