Cerebral Amyloid Angiopathy

Table of Contents

1. Amyloid in the Walls of Brain Arteries
2. How Common It Is
3. The Link to Alzheimer's Disease
4. Lobar Brain Bleeds and the Risk of a Repeat Bleed
5. Microbleeds and Cortical Superficial Siderosis on Brain Scans
6. Transient Focal Neurological Episodes (Amyloid Spells)
7. The Boston Criteria Version 2.0 (2022)
8. The Inflammatory Form and Its Response to Steroids
9. Hereditary and Transmitted Forms
10. Anti-Amyloid Antibody Drugs and Imaging Abnormalities
11. What Studies Report About Blood Thinners and Blood Pressure
12. Key Research Papers
13. Connections
14. Featured Videos

Amyloid in the Walls of Brain Arteries

Every brain makes amyloid-beta all the time. It is a short piece cut from a larger protein that sits in the outer skin of nerve cells. In a healthy brain the fragment is cleared away — partly by being broken down, and partly by draining out along the walls of small arteries, in the thin channels that carry fluid away from brain tissue. A 2020 review by Steven Greenberg and colleagues in Nature Reviews Neurology describes cerebral amyloid angiopathy and Alzheimer's disease as two diseases driven by the same failure: amyloid-beta is not cleared fast enough. When it builds up along those drainage routes it sticks to the vessel wall itself.

The arteries affected are small ones on the surface of the brain (the leptomeningeal arteries, which run in the thin membranes covering the brain) and the small arteries that dive from the surface into the outer layer of the brain, the cortex. Amyloid replaces the muscle cells that normally give an artery wall its strength and its ability to widen and narrow. A vessel packed with amyloid behaves more like a glass tube than a living pipe. The review describes a self-reinforcing cycle: more amyloid in the vessel wall slows drainage further, which leaves more amyloid behind to collect in both the vessel and the surrounding brain.

This is why the disease favours the outer parts of the brain and its lobes — the back of the head (occipital lobe) and the sides and top (parietal lobe) in particular — rather than the deep structures in the middle of the brain. That pattern matters, because the other common cause of small-vessel bleeding, long-standing high blood pressure, tends to damage the deep arteries instead. Doctors use the location of bleeds on a scan to tell the two apart.

The damage shows up in three main ways:

• Bleeds, from tiny pinpoint leaks to large bleeds inside a lobe of the brain.
• Small areas of poor blood supply, because stiff vessels cannot deliver blood as well, which shows up as scarring in the white matter (the wiring between brain regions).
• Slowly worsening thinking and memory, either on its own or alongside Alzheimer's disease.

How Common It Is

Cerebral amyloid angiopathy cannot be seen directly while a person is alive; it is confirmed by looking at brain tissue under a microscope, usually after death. During life it is estimated from signs on a magnetic resonance imaging (MRI) scan, especially tiny bleeds that sit only in the outer parts of the brain. The two methods give different numbers, and a large 2022 study pulled them together.

Lieke Jäkel and colleagues at Radboud University in the Netherlands combined 170 studies covering more than 73,000 people. They found:

• In the general population, tissue studies found the disease in 23% of people, while brain-scan signs found it in 7% — a three-fold difference, meaning scans miss many cases.
• In older people with normal thinking, both methods agreed on roughly 5% to 7%.
• In people with Alzheimer's disease, tissue studies found it in 48%, about twice the 22% found by scans.
• In people who had a bleed inside the brain of any kind, both methods found it in roughly 19% to 24%.
• In people whose bleed sat in a lobe of the brain (a lobar bleed), both methods found it in roughly 50% to 57%.

The authors noted large differences between the methods used by different research teams and called for standard ways of measuring and reporting the disease.

The disease is closely tied to age. The 2022 international team that updated the diagnostic criteria described it as "an age-related small vessel disease" marked by "progressive deposition" of amyloid-beta in the vessel wall, and their criteria apply only to people aged 50 years and older. The sporadic (non-inherited) form is rarely diagnosed before that age; when it appears in younger people, doctors look for an inherited or acquired cause, described further down this page.

The Link to Alzheimer's Disease

Cerebral amyloid angiopathy and Alzheimer's disease are built from the same protein. In Alzheimer's disease the amyloid-beta clumps into plaques between nerve cells; in cerebral amyloid angiopathy it collects in the vessel wall. The two very often appear together: in the Jäkel meta-analysis, nearly half of people with Alzheimer's disease (48%) had the vessel disease when their brain tissue was examined.

The Greenberg review explains why the two can still look different. Slightly different lengths of the amyloid-beta fragment, and other proteins that settle alongside it, push it toward either the vessel wall or the plaques. The two diseases also injure the brain in different ways — the plaque disease mainly through nerve-cell damage and the tangle protein tau, the vessel disease mainly through bleeding and poor blood flow.

A 2022 pooled analysis of 46 hospital studies by Kunal Malhotra and colleagues, covering 7,159 patients with cerebral amyloid angiopathy, found mild cognitive impairment or dementia in about half (50%). The same gene variant that raises the risk of Alzheimer's disease — the ε4 form of the apolipoprotein E gene — is also tied to the vessel disease and to the side effects of the newer anti-amyloid drugs, as the sections below describe.

Lobar Brain Bleeds and the Risk of a Repeat Bleed

The most serious result of cerebral amyloid angiopathy is a bleed inside the brain, called an intracerebral hemorrhage. The bleeds caused by this disease sit in a lobe of the brain, close to the surface, rather than deep in the middle. A lobar bleed causes sudden symptoms that depend on where it is: weakness or numbness on one side, trouble speaking or understanding, loss of part of the field of vision, a sudden severe headache, confusion, a seizure, or drowsiness. Hospitals treat any of these sudden signs as an emergency, because a bleed and a clot-type stroke look the same from the outside and need a brain scan to tell apart.

What sets this disease apart is how often the bleeding comes back. Andreas Charidimou and colleagues pooled 10 studies in 2017 that followed 1,306 survivors of a bleed inside the brain, each scanned soon after the bleed:

• In 325 patients whose bleed was linked to cerebral amyloid angiopathy, a new bleed occurred in about 7.4% per year.
• In 981 patients whose bleed had another cause, the figure was about 1.1% per year.
• Among the amyloid-related cases, several tiny bleeds on the first scan were tied to a higher chance of another bleed — roughly three to four times higher for people with 2–4, 5–10, or more than 10 tiny bleeds, compared with none.
• A single tiny bleed was not tied to a higher risk in either group.

A seven-fold difference in the yearly risk of another bleed is the main reason doctors work hard to find out whether a lobar bleed was caused by this disease.

Microbleeds and Cortical Superficial Siderosis on Brain Scans

Most of what is known about cerebral amyloid angiopathy in living people comes from special magnetic resonance imaging sequences that are very sensitive to old blood. When blood leaks out of a vessel, the iron in it stays behind for years as a rust-like deposit called hemosiderin. On these scans it shows up as a small black dot or a dark line.

Microbleeds

A cerebral microbleed is a tiny leak that often causes no symptoms at all. In the Malhotra meta-analysis, microbleeds were seen in 52% of patients with cerebral amyloid angiopathy. Microbleeds that sit only in the lobes and the outer layer of the brain point toward this disease; microbleeds deep in the middle of the brain point toward damage from high blood pressure.

Cortical superficial siderosis

Cortical superficial siderosis is a thin coating of old blood along the surface folds of the brain. It comes from small bleeds into the space just outside the brain (a convexity subarachnoid hemorrhage) that run along the grooves between brain folds. Malhotra and colleagues found it in 49% of patients with the disease, and it was the only scan sign tied to a higher chance of another bleed (odds ratio 1.57).

A 2019 meta-analysis by Charidimou and colleagues looked at this sign closely in 1,239 patients from 6 studies who were followed for an average of 3.1 years:

• About 34% of the patients had the sign.
• The yearly rate of a symptomatic bleed was 3.9% without the sign and 11.1% with it.
• When the coating was limited to three or fewer brain grooves (focal), the yearly rate was 9.1%; when it was spread over more than three (disseminated), it was 12.5%.
• After adjusting for other factors, any coating roughly doubled the risk of a future bleed, and the spread-out pattern roughly quadrupled it (hazard ratio 4.28).

The authors called the presence and extent of this coating the most important scan sign for predicting future bleeds.

White-matter signs

The same hospital studies often show changes in the brain's wiring. In the Malhotra analysis, enlarged fluid spaces around the small vessels near the top of the brain (in an area called the centrum semiovale) were seen in 56% of patients, and moderate or severe white-matter scarring in 53%. These signs became part of the updated diagnostic criteria in 2022.

Transient Focal Neurological Episodes (Amyloid Spells)

Some people with cerebral amyloid angiopathy have short, repeated spells of tingling, numbness, weakness, or visual disturbance that come and go within minutes. Doctors call these transient focal neurological episodes, and they are often nicknamed "amyloid spells." They are easily mistaken for a mini-stroke (a transient ischemic attack) or for a migraine aura.

Charidimou and colleagues described the range of these spells in 2012 in a study of 172 patients from several centres, together with a review of every published case:

• 25 of the 172 patients (14.5%) had such spells.
• About half had "positive" symptoms, such as tingling that spreads across the body like a migraine aura, flashing lights, or limb jerking; the other half had "negative" symptoms, such as sudden weakness, trouble speaking, or loss of vision, which look like a mini-stroke.
• Patients with spells more often had cortical superficial siderosis or a small surface bleed on the scan (50% versus 19% in patients without spells), and the authors proposed that these surface bleeds cause the spells.
• Over a median of 14 months, half of the patients with spells went on to have a symptomatic lobar bleed. The pooled data put the risk of a bleed at 24.5% within 8 weeks of a spell.

A 2022 review by José María Sánchez-Caro and colleagues gathered 248 patients with these spells from 42 published studies and one hospital cohort. Over a median follow-up of one year:

• 76 patients (39.4%) had a symptomatic lobar bleed.
• Spells involving movement or weakness were tied to about twice the odds of a later bleed.
• Taking blood-thinning medicines (antithrombotics) after a spell was tied to about 3.6 times the odds of a later bleed. The authors noted that in many cases these medicines had been started because the spell was mistaken for a mini-stroke.
• 31 patients (16.5%) died during follow-up; a later lobar bleed and cortical superficial siderosis were the main factors tied to death.

The authors concluded that telling these spells apart from transient ischemic attacks is critical. The pooled prevalence of the spells varies a great deal between studies: the Malhotra analysis found them in 48% of hospital patients overall, but in only 17% in the prospective studies, compared with 57% in the retrospective ones.

The Boston Criteria Version 2.0 (2022)

Because the disease can only be proven with brain tissue, doctors use a set of scan-based rules called the Boston criteria to say how likely it is. The rules were first developed at Massachusetts General Hospital in Boston and had last been updated in 2010. In 2022 an international team led by Andreas Charidimou and Steven Greenberg published version 2.0 in The Lancet Neurology, adding newer scan signs.

The study looked at patients aged 50 years and older who had a spontaneous brain bleed, thinking problems, or transient focal neurological episodes, and who had both a magnetic resonance imaging scan and brain tissue to check the diagnosis against. The team built the rules from 159 Boston patients and then tested them on two separate groups (59 later Boston patients and 123 patients from other centres in North America and Europe).

Under version 2.0, "probable" cerebral amyloid angiopathy requires, in a person aged 50 or older, either:

• at least two bleeding signs found only in the lobes and outer brain — any mix of lobar brain bleeds, microbleeds, or patches of cortical superficial siderosis; or
• one such bleeding sign plus one white-matter sign: severe enlarged fluid spaces around the small vessels in the centrum semiovale, or white-matter scarring in a "multispot" pattern.

How the new rules performed:

• Among all patients with a full autopsy, version 2.0 picked up 74.5% of true cases (sensitivity), compared with 64.5% for the older rules.
• It correctly ruled out the disease in 95.0% of those without it (specificity), the same as the older rules.
• Overall accuracy, measured as the area under the curve, was 0.848 for version 2.0 against 0.798 for the older rules, a statistically significant gain.

The authors noted that further studies are needed to see how well the criteria work across all kinds of patients.

The Inflammatory Form and Its Response to Steroids

In a small group of patients, the body's immune system reacts against the amyloid in the vessel walls. This is called cerebral amyloid angiopathy-related inflammation. It can cause headache, confusion, a change in behaviour, seizures, or weakness, and the scan shows swelling in the white matter, often more on one side, alongside the usual microbleeds.

The Boston series

Robert Regenhardt and colleagues at Massachusetts General Hospital followed 48 consecutive patients with this form for a median of 2.7 years, reporting in 2020. Their mean age was 68.9 years.

• 94% had white-matter swelling on the scan (73% of those on one side more than the other), and 87% had microbleeds.
• After the first episode, 69% received corticosteroids, 13% cyclophosphamide, and 4% mycophenolate; 29% received no immune-suppressing treatment.
• Clinical improvement occurred in 94% of treated patients and 50% of untreated patients; the scan improved in 86% and 29%.
• The illness came back in 26% of treated patients and 71% of untreated patients (hazard ratio 0.19).

The authors wrote that the results support the effectiveness of immune-suppressing treatment and suggest that early treatment may improve the first episode and lower the chance of it coming back. The study was observational, not a randomised trial.

The international registry

Laura Antolini, Fabrizio Piazza and colleagues followed 113 patients in an international network from 2013 to 2017, reporting in 2021. Their mean age was 72.9 years, 37.1% carried the ε4 gene variant, and 36.3% had a history of Alzheimer's disease.

• After the first episode, 70.3% had recovered clinically within 3 months and 84.1% within 12 months; the scan had cleared in 45.1% and 77.4% at those times.
• Within the following 24 months, 38.3% had at least one relapse.
• A relapse was more likely when high-dose intravenous steroid pulses were stopped suddenly than when they were followed by a slow tapering of oral steroids (hazard ratio 4.68).

The authors described the scan changes in this condition as "spontaneous ARIA-like events," because they look very much like the side effects seen with the anti-amyloid antibody drugs described below.

Hereditary and Transmitted Forms

The Dutch type

A rare inherited form, first described in Dutch families, is known as hereditary cerebral hemorrhage with amyloidosis, Dutch type, or Dutch-type cerebral amyloid angiopathy. In 1990 Efrat Levy, Blas Frangione and colleagues reported in Science that the amyloid in these patients' vessel walls is the same as the amyloid of Alzheimer's disease, and that affected people carry a single-letter change in the gene for the amyloid precursor protein. The change swaps one building block (glutamic acid) for another (glutamine) at position 22 of the amyloid-beta fragment. The authors linked the change to amyloid buildup in the vessel walls, brain bleeds, and early death.

Because carriers can be identified before symptoms begin, the Dutch type gives researchers a way to watch the disease from its earliest stage. In 2020 Emma Koemans and colleagues in the Netherlands studied 86 carriers (mean age 57):

• 56% had migraine, all of it with aura — more than expected for the general population.
• Migraine was the first symptom in 77% of carriers with it, and the only symptom in 35%.
• The time between the start of migraine and the first brain bleed was 8.5 years.
• An aura lasting 60 minutes or longer signalled an acute brain bleed in 55% of such attacks.

The transmitted form

A newer line of research suggests amyloid-beta can, rarely, be passed from one person to another through medical treatment. In 2015 Zane Jaunmuktane, John Collinge, Sebastian Brandner and colleagues reported in Nature on 8 people, aged 36 to 51, who had died of Creutzfeldt-Jakob disease after childhood treatment with growth hormone taken from the pituitary glands of dead donors. Four of them had moderate to severe amyloid-beta in the brain, including amyloid in the vessel walls typical of cerebral amyloid angiopathy — unusual for their age and not explained by known risk genes. The authors described the findings as consistent with transmission of amyloid-beta along with the prions. The Stanley Prusiner page covers this work and the prion research behind it.

Anti-Amyloid Antibody Drugs and Imaging Abnormalities

The antibody drugs for early Alzheimer's disease — aducanumab, lecanemab and donanemab — are designed to clear amyloid-beta from the brain. Their main side effect is a set of scan changes called amyloid-related imaging abnormalities (ARIA). These come in two kinds: swelling or fluid leakage in the brain (the "edema" type), and new microbleeds or new cortical superficial siderosis (the "hemosiderin" type). The Greenberg review describes amyloid-related imaging abnormalities as a probable meeting point of the two diseases: when the drugs pull amyloid out of plaques, the drainage routes along the vessel walls become overloaded, and vessels already damaged by cerebral amyloid angiopathy leak.

What the trials reported

• Aducanumab. In the combined EMERGE and ENGAGE trials (3,285 participants), Stephen Salloway and colleagues reported that 41.3% of people on the high dose (10 mg per kilogram) had amyloid-related imaging abnormalities, with serious cases in 1.4%. The swelling type occurred in 35.2% (2.7% on placebo), and about a quarter of those had symptoms, most often headache, confusion, dizziness and nausea. New microbleeds occurred in 19.1% and new superficial siderosis in 14.7%. The swelling type was most common in carriers of the ε4 gene variant, and 98.2% of swelling events cleared on later scans.
• Lecanemab. In the 18-month Clarity AD trial of 1,795 people, which gave lecanemab 10 mg per kilogram into a vein every 2 weeks, Christopher van Dyck and colleagues reported the swelling or fluid type in 12.6% of people on the drug. Decline on the main memory-and-function score was 0.45 points less than with placebo on an 18-point scale.
• Donanemab. In the TRAILBLAZER-ALZ 2 trial of 1,736 people, John Sims and colleagues reported the swelling or fluid type in 24.0% on donanemab (52 people with symptoms) and 2.1% on placebo. Three deaths in the donanemab group and one in the placebo group were considered treatment related.

Who was at higher risk

A 2025 analysis of 3,030 participants in the donanemab trials by Jennifer Zimmer and colleagues found the swelling type in 24.4% and the microbleed type in 31.3% of people on the drug in the placebo-controlled trials, compared with 1.9% and 13.0% on placebo. Serious swelling occurred in 1.5%, and in 58.3% of those who developed swelling the first event came by the third infusion. The higher-risk features were:

• more copies of the ε4 gene variant;
• a larger number of microbleeds on the starting scan;
• cortical superficial siderosis on the starting scan;
• more amyloid plaque;
• higher blood pressure. Taking blood-pressure medicine was tied to a lower risk.

Several of these are the same scan signs used to diagnose cerebral amyloid angiopathy. The Jäkel team gave the link to these side effects as one reason that knowing how common the vessel disease is matters. The regulatory history of each drug is covered on the aducanumab, lecanemab and donanemab pages.

What Studies Report About Blood Thinners and Blood Pressure

No medicine has been shown to remove amyloid from the vessel walls in this disease. Research after a bleed has focused on two questions: what blood-thinning medicines do, and what lowering blood pressure does.

Blood-pressure lowering: the PROGRESS trial

PROGRESS was a placebo-controlled trial of 6,105 people with cerebrovascular disease (earlier problems with the blood vessels of the brain). It gave perindopril to everyone in the treatment group, plus the water pill indapamide for those who had neither a clear need for nor a reason against a water pill. In a 2010 follow-up analysis, Hisatomi Arima and colleagues counted bleeds over a mean of 3.9 years:

• There were 16 probable amyloid-related bleeds, 51 probable blood-pressure-related bleeds and 44 unclassified bleeds.
• Active treatment lowered the risk of amyloid-related bleeds by 77% and blood-pressure-related bleeds by 46%.
• The effect did not differ clearly between the types of bleed, and the authors concluded that blood-pressure lowering is likely to protect against all types.

The amyloid-related result rests on only 16 events, so the range of possible effect was wide (19% to 93%). The donanemab analysis above also found that blood-pressure medicine was tied to fewer amyloid-related imaging abnormalities.

Antiplatelet medicines: the RESTART trial

RESTART was a trial at 122 hospitals in the United Kingdom of 537 people who had a bleed inside the brain while taking a blood thinner to prevent clots. A median of 76 days after the bleed, half were assigned to start an antiplatelet medicine (such as aspirin) and half to stay off it. Over a median of 2 years, reporting in 2019:

• 12 of 268 people (4%) who started antiplatelet medicine had another brain bleed, compared with 23 of 268 (9%) who stayed off it. This difference was not statistically significant (hazard ratio 0.51, 95% confidence interval 0.25–1.03).
• Major clot-type (occlusive) vascular events were about equal: 15% and 14%.
• The investigators concluded that the results exclude all but a very modest increase in the risk of another bleed with antiplatelet medicine.

A planned subgroup analysis by Rustam Al-Shahi Salman and colleagues looked at the 254 participants who had the required magnetic resonance imaging scan. Antiplatelet medicine showed no clear harm in people with two or more microbleeds, or with microbleeds only in the lobes — the pattern linked to cerebral amyloid angiopathy. The authors called for larger trials to confirm this, because the numbers in these subgroups were small.

Blood thinners after amyloid spells

In the Sánchez-Caro review of transient focal neurological episodes, blood-thinning medicines taken after a spell were tied to about 3.6 times the odds of a later lobar bleed. That was an observational finding in a group that is already at high risk, and many of those medicines had been started because the spell was mistaken for a mini-stroke.

Anticoagulants (the stronger blood thinners used for atrial fibrillation) are a separate question. RESTART tested antiplatelet medicines only and did not answer it. Decisions about blood thinners after a brain bleed involve weighing bleeding risk against clot risk and belong with the treating clinicians.

Key Research Papers

1. Jäkel L, De Kort AM, Klijn CJM, et al. Prevalence of cerebral amyloid angiopathy: A systematic review and meta-analysis. Alzheimers Dement. 2022;18(1):10-28. PubMed PMID: 34057813
2. Charidimou A, Boulouis G, Frosch MP, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI-neuropathology diagnostic accuracy study. Lancet Neurol. 2022;21(8):714-725. PubMed PMID: 35841910
3. Charidimou A, Imaizumi T, Moulin S, et al. Brain hemorrhage recurrence, small vessel disease type, and cerebral microbleeds: A meta-analysis. Neurology. 2017;89(8):820-829. PubMed PMID: 28747441
4. Greenberg SM, Bacskai BJ, Hernandez-Guillamon M, et al. Cerebral amyloid angiopathy and Alzheimer disease - one peptide, two pathways. Nat Rev Neurol. 2020;16(1):30-42. PubMed PMID: 31827267
5. Malhotra K, Theodorou A, Katsanos AH, et al. Prevalence of Clinical and Neuroimaging Markers in Cerebral Amyloid Angiopathy: A Systematic Review and Meta-Analysis. Stroke. 2022;53(6):1944-1953. PubMed PMID: 35264008
6. Charidimou A, Boulouis G, Greenberg SM, et al. Cortical superficial siderosis and bleeding risk in cerebral amyloid angiopathy: A meta-analysis. Neurology. 2019;93(24):e2192-e2202. PubMed PMID: 31732564
7. Charidimou A, Peeters A, Fox Z, et al. Spectrum of transient focal neurological episodes in cerebral amyloid angiopathy: multicentre magnetic resonance imaging cohort study and meta-analysis. Stroke. 2012;43(9):2324-30. PubMed PMID: 22798323
8. Sanchez-Caro JM, de Lorenzo Martínez de Ubago I, de Celis Ruiz E, et al. Transient Focal Neurological Events in Cerebral Amyloid Angiopathy and the Long-term Risk of Intracerebral Hemorrhage and Death: A Systematic Review and Meta-analysis. JAMA Neurol. 2022;79(1):38-47. PubMed PMID: 34779831
9. Regenhardt RW, Thon JM, Das AS, et al. Association Between Immunosuppressive Treatment and Outcomes of Cerebral Amyloid Angiopathy-Related Inflammation. JAMA Neurol. 2020;77(10):1261-1269. PubMed PMID: 32568365
10. Antolini L, DiFrancesco JC, Zedde M, et al. Spontaneous ARIA-like Events in Cerebral Amyloid Angiopathy-Related Inflammation: A Multicenter Prospective Longitudinal Cohort Study. Neurology. 2021;97(18):e1809-e1822. PubMed PMID: 34531298
11. Levy E, Carman MD, Fernandez-Madrid IJ, et al. Mutation of the Alzheimer's disease amyloid gene in hereditary cerebral hemorrhage, Dutch type. Science. 1990;248(4959):1124-6. PubMed PMID: 2111584
12. Koemans EA, Voigt S, Rasing I, et al. Migraine With Aura as Early Disease Marker in Hereditary Dutch-Type Cerebral Amyloid Angiopathy. Stroke. 2020;51(4):1094-1099. PubMed PMID: 32114932
13. Jaunmuktane Z, Mead S, Ellis M, et al. Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature. 2015;525(7568):247-50. PubMed PMID: 26354483
14. Salloway S, Chalkias S, Barkhof F, et al. Amyloid-Related Imaging Abnormalities in 2 Phase 3 Studies Evaluating Aducanumab in Patients With Early Alzheimer Disease. JAMA Neurol. 2022;79(1):13-21. PubMed PMID: 34807243
15. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in Early Alzheimer's Disease. N Engl J Med. 2023;388(1):9-21. PubMed PMID: 36449413
16. Sims JR, Zimmer JA, Evans CD, et al. Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial. JAMA. 2023;330(6):512-527. PubMed PMID: 37459141
17. Zimmer JA, Ardayfio P, Wang H, et al. Amyloid-Related Imaging Abnormalities With Donanemab in Early Symptomatic Alzheimer Disease: Secondary Analysis of the TRAILBLAZER-ALZ and ALZ 2 Randomized Clinical Trials. JAMA Neurol. 2025;82(5):461-469. PubMed PMID: 40063015
18. Arima H, Tzourio C, Anderson C, et al. Effects of perindopril-based lowering of blood pressure on intracerebral hemorrhage related to amyloid angiopathy: the PROGRESS trial. Stroke. 2010;41(2):394-6. PubMed PMID: 20044530
19. RESTART Collaboration. Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial. Lancet. 2019;393(10191):2613-2623. PubMed PMID: 31128924
20. Al-Shahi Salman R, Minks DP, Mitra D, et al. Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial. Lancet Neurol. 2019;18(7):643-652. PubMed PMID: 31129065

PubMed Topic Searches

1. PubMed: cerebral amyloid angiopathy
2. PubMed: Boston criteria 2.0
3. PubMed: cortical superficial siderosis
4. PubMed: transient focal neurological episodes
5. PubMed: cerebral amyloid angiopathy-related inflammation
6. PubMed: amyloid-related imaging abnormalities

Connections

• Vascular Dementia — the parent page on small-vessel brain disease
• Alzheimer's Disease — the same amyloid-beta protein, deposited as plaques
• Stroke — bleeding and clot-type strokes
• CADASIL — another inherited small-vessel disease of the brain
• Taxifolin — the flavonoid studied in a mouse model of this disease
• Stanley Prusiner — prions and the transmitted amyloid-beta findings
• Lecanemab Full Approval (2023) — the regulatory record of an anti-amyloid antibody
• Donanemab Approval (2024) — the regulatory record and its imaging side effects

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