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Transmission of Cerebral β-Amyloidosis Among Individuals
Tsuyoshi Hamaguchi1, Kenjiro Ono2, Masahito Yamada3,4
1Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, 920-8640, Japan. gom56@med.kanazawa-u.ac.jp.
Abstract:
Deposition of amyloid β protein (Aβ) in the brain (cerebral β-amyloidosis) is a hallmark of Alzheimer's disease (AD). So far, there have been increasing number of experimental studies using AD mouse model that cerebral β-amyloidosis could be transmitted among individuals as prion-like mechanism. Furthermore, several pathological studies using autopsied patients with iatrogenic Creutzfeldt-Jakob disease (CJD) showed that cerebral β-amyloidosis in addition to the CJD pathology could be transmitted among humans via medical procedures, such as human growth hormone derived from cadaver injection and cadaveric dura mater graft. In addition, although cerebral amyloid angiopathy (CAA), which is Aβ deposition in the cerebral vessels, related cerebral hemorrhage rarely develops in young people, several patients with CAA-related cerebral hemorrhage under the age of 55 with histories of neurosurgeries with and without dura mater graft in early childhood have been reported. These patients might show that Aβ pathology is often recognized as Aβ-CAA rather than parenchymal Aβ deposition in the transmission of cerebral β-amyloidosis in humans, and we proposed an emerging concept, "acquired CAA". Considering that there have been several patients with acquired CAA with an incubation period from neurosurgery and the onset of CAA related cerebral hemorrhage of longer than 40 years, the number of cases is likely to increase in the future, and detailed epidemiological investigation is required. It is necessary to continue to elucidate the pathomechanisms of acquired CAA and urgently establish a method for preventing the transmission of cerebral β-amyloidosis among individuals.
Insights
Alzheimer's disease protein (Aβ) can spread like prions, potentially transmitted via medical procedures. This research highlights acquired cerebral amyloid angiopathy (CAA) as a concerning, transmissible condition.
Area of Science:
- Neuroscience
- Pathology
- Epidemiology
Background:
- Cerebral β-amyloidosis, a hallmark of Alzheimer's disease (AD), is increasingly studied for prion-like transmission.
- Studies suggest human growth hormone and dura mater grafts can transmit amyloid β protein (Aβ) pathology.
- Cerebral amyloid angiopathy (CAA) related cerebral hemorrhage has been observed in young patients with histories of neurosurgery.
Purpose of the Study:
- To explore the prion-like transmission of cerebral β-amyloidosis.
- To investigate the concept of "acquired CAA" resulting from medical procedures.
- To emphasize the need for epidemiological studies and transmission prevention methods.
Main Methods:
- Review of experimental studies using AD mouse models.
- Analysis of pathological studies on autopsied patients with iatrogenic Creutzfeldt-Jakob disease (CJD).
- Examination of case reports of young patients with CAA-related cerebral hemorrhage and neurosurgical histories.
Main Results:
- Evidence supports the prion-like transmission of cerebral β-amyloidosis.
- Aβ pathology, particularly Aβ-CAA, can be transmitted among humans.
- Long incubation periods (over 40 years) are observed for acquired CAA following neurosurgery.
Conclusions:
- Cerebral β-amyloidosis, including acquired CAA, poses a transmissible risk.
- Detailed epidemiological investigation is crucial due to the likely increase in acquired CAA cases.
- Developing methods to prevent Aβ transmission is urgently needed.
