Is AD Transmissible? The Evidence for ‘Iatrogenic’ Disease

Alzheimer’s disease (AD) is not contagious. It cannot be caught through touching, caring for, living with, or otherwise having routine contact with someone who has the disease.But a small and growing body of evidence suggests that, in rare circumstances, amyloid-beta pathology associated with AD — and possibly AD itself — may be transmitted from one person to another through certain medical procedures including childhood injections of cadaver-derived growth hormone (c-hGH), dura mater grafts, and reused neurosurgical instruments.What evidence supports the existence of iatrogenic AD, what remains speculative, and how should clinicians discuss the findings with concerned patients?What’s the Claim — and Where Did It Come From?The story has its roots in prion disease.Before recombinant growth hormone became available, thousands of children with growth hormone deficiency were treated with c-hGH. Some preparations were inadvertently contaminated with prions that cause Creutzfeldt-Jakob disease (CJD), leading to more than 200 cases of iatrogenic CJD among c-hGH recipients worldwide. Use of c-hGH was halted in 1985.In 2015, researchers at University College London (UCL), London, England, examined the brains of eight people, aged 36-51 years, who died from iatrogenic CJD after receiving c-hGH.Four had moderate-to-severe amyloid-beta deposits in brain tissue and blood vessels — an unusually heavy amyloid burden for their age. None carried the APOE epsilon 4 genotype or known mutations that would readily explain such early amyloid-beta pathology. The researchers proposed that the c-hGH preparations might have contained amyloid-beta “seeds” capable of triggering further amyloid-beta aggregation in recipients.In 2018, the UCL team found amyloid-beta40, amyloid-beta42, and tau proteins in archived samples of the implicated c-hGH preparations. When material from some of those batches was injected into genetically susceptible mice, it seeded amyloid-beta plaques and cerebral amyloid angiopathy (CAA) — “consistent with the hypothesized iatrogenic human transmission of amyloid-beta pathology,” they wrote in Nature.The possibility that iatrogenic amyloid-beta transmission might lead to AD itself gained attention in 2024, when the UCL group described eight additional c-hGH recipients.Five had developed progressive early-onset dementia, generally beginning between ages 38 and 55, and one had mild cognitive impairment (MCI). The interval between c-hGH exposure and cognitive symptoms was roughly 30-40 years. Two patients had biomarker findings consistent with AD. Genetic testing provided no clear alternative explanation for the unusually early disease.What Changed in 2026?A major limitation of the 2024 iatrogenic AD report was that none of the dementia cases had definitive AD neuropathology confirmed at autopsy.The 2024 cases were “extremely complicated” clinically, making it difficult to draw “a direct line between the seeding and what you would call Alzheimer’s disease,” Lary Walker, PhD, associate professor, emeritus, Department of Neurology, Emory University School of Medicine, Atlanta, noted in an interview with Medscape Medical News.For example, the recipients had a variety of premorbid neurologic conditions that led to the need for hGH, some of which could potentially complicate interpretation of their later cognitive and neurologic symptoms, he explained.The evidence gap narrowed in March 2026, when the UCL team published a case report of a c-hGH recipient with early-onset dementia, in whom postmortem examination showed “unequivocal” neuropathological features of AD, including severe tauopathy.The male patient was treated with c-hGH during childhood and developed cognitive symptoms at age 47. He developed progressive dementia with prominent language problems and died at 57. Genetic testing found no pathogenic variants in AD-associated genes. At autopsy, his brain showed extensive parenchymal amyloid-beta pathology, severe and widespread CAA, and extensive tau pathology — “corresponding to the highest level of AD neuropathological change,” the researchers wrote in JAMA Neurology. They acknowledged, however, that there are inherent challenges in proving causality in iatrogenic AD.What Other Routes Are Under Study?Cadaveric growth hormone is not the only historical exposure linked to amyloid-beta transmission. Cases of iatrogenic CAA have been described decades after patients received cadaveric dura mater grafts during neurosurgery. amyloid-beta can accumulate in dura, providing a biologically plausible source of amyloid-beta seeds.A 2026 scoping review identified 94 published cases of possible iatrogenic CAA. Cranial surgery was the predominant exposure and cadaveric dura mater was documented in 44 cases. The median age at exposure was 4 years, with a median latency of 36 years before presentation, and acute intracerebral hemorrhage (ICH) was the first presentation in more than half the cases.Another suspected route is reused neurosurgical equipment. Reports have described patients who developed unusually early CAA decades after childhood neurosurgery even when exposure to cadaveric dura could not be established. Four such patients reported in 2018 developed ICH about 3 decades after childhood or adolescent neurosurgery, raising the possibility that contaminated instruments could have transferred amyloid-beta seeds.The newest and perhaps most speculative possibility is blood transfusion.In a 2023 Scandinavian study of more than 1 million transfusion recipients, patients receiving red blood cells from donors who later experienced multiple spontaneous ICH had more than twice the risk of subsequently developing a spontaneous ICH themselves. Because recurrent lobar hemorrhage can be a manifestation of CAA, the authors raised the possibility of a transfusion-transmissible factor.But the study did not determine whether donors or recipients actually had CAA, did not measure amyloid-beta in blood products, and could not establish that anything was transmitted. Selection bias, residual confounding, or another mechanism could explain the association, the authors cautioned.A separate Scandinavian study of nearly 1.5 million transfusion recipients found no evidence that receiving blood from donors who later developed AD increased recipients’ risk for AD.What Do Skeptics Say?Walker’s overall view is that the evidence for iatrogenic AD has strengthened but remains far from definitive. The autopsy-confirmed case “doesn’t change things a whole lot,” largely because these cases are “extraordinarily rare,” he said. Transmission of amyloid-beta as a leading causing CAA is well established, he noted, but whether the same phenomenon can produce full AD is still “an open question.”Brian Appleby, MD, and Mark Cohen, MD, with the National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, similarly emphasized the remaining uncertainty in an editorial accompanying the 2026 autopsy case report. Evidence for medically acquired amyloid-beta pathology and CAA is considerably stronger than evidence that AD itself can be transmitted, they noted.In a 2024 Nature Medicine commentary, Walker and Mathias Jucker, PhD, of the German Center for Neurodegenerative Diseases, Tübingen, Germany, said there is “credible” evidence that, under extraordinary circumstances, AD may be transmitted through a prion-like mechanism. But exactly how transmitted amyloid-beta pathology might lead to tau pathology and dementia remains uncertain.Walker was cautious about blood transfusion as a possible transmission route. He characterized the current evidence as largely indirect, noting that researchers “really haven’t shown a direct link” connecting prior transfusion, subsequent hemorrhage, and amyloid-beta seeds.“There’s no direct evidence that this is a seeding mechanism in those cases,” but the issue warrants continued study and attention to potential safeguards, he said.The authors of a Lancet Viewpoint agreed that the blood-transfusion hypothesis requires much stronger evidence. They called for epidemiologic replication and studies capable of determining whether amyloid-beta seeds are present in blood, whether they retain seeding activity in blood products, and whether particular donor or recipient characteristics influence any risk.What Should Clinicians Tell Patients?The most important messages are that these reports do not show that AD is contagious and that the exposures providing the strongest evidence are largely historical, Walker said. c-hGH was discontinued in 1985 after the CJD risk became apparent, and recombinant growth hormone replaced it. In the UK, use of cadaveric dura mater was discontinued in 1992.Reused surgical instruments pose a more complicated theoretical issue. Standard sterilization is highly effective against conventional infectious organisms, but prions are unusually resistant. CDC guidance therefore recommends special decontamination procedures when instruments have contacted tissue from patients with suspected or confirmed CJD.With regard to blood transfusion, Walker said there may be ways to reduce the already low risk even further, pointing to white blood cell depletion used to reduce transmission risk in prion disease as one example.Age limits on blood donation may be worthy of consideration, Walker said, although he acknowledged that this could be difficult because blood donation is already down and donors tend to be older.He emphasized that patients should not interpret the current evidence to mean that routine surgery or blood transfusion carries a demonstrated risk for AD. When asked whether patients should be reassured rather than worried, he was emphatic: “Absolutely.”What Comes Next?The International Registry for Iatrogenic Cerebral Amyloid Angiopathy, established in January 2024, included 124 patients from 11 countries as of 2025. The registry is designed to collect cases internationally and characterize clinical presentation, natural history, and potential causative exposures.A separate UK registry for iatrogenic CAA plans to identify cases through nationwide surveys of neurologists and stroke physicians.Experts have also called for multidisciplinary collaboration across neurology, neurosurgery, infectious disease, and transplant medicine to help mitigate potential iatrogenic CAA risk.Walker reported having no relevant disclosures.