Evidence Suggesting That Alzheimer's Disease May Be a Transmissible Disorder

Overview

Journal Int J Mol Sci

Publisher MDPI

Date 2025 Jan 25

PMID 39859223

Authors

Genevieve Saw

Ling-Xiao Yi

Eng King Tan

Zhi Dong Zhou

Affiliations

Soon will be listed here.

Abstract

Alzheimer's disease (AD) is characterised by progressive neurodegeneration with the formation of amyloid beta (Aβ) plaques and neurofibrillary tau tangles in the brain parenchyma. The causes of AD have been attributed to a combination of age-related changes within the brain as well as genetic, environmental and lifestyle factors. However, a recent study by Banerjee et al. highlights the possibility that AD may be a transmissible disease and that iatrogenic AD could be environmentally acquired, similar to iatrogenic Creutzfeldt-Jakob disease (iCJD). The study reports that contaminated Aβ in cadaver-derived pituitary growth hormone (c-hGH) therapy, which patients received during childhood inoculation, may accidentally transmit into their brains, triggering neurodegeneration and AD onset in older age. Furthermore, corroborating evidence from various animal model studies and human case reports suggests that AD can be potentially transmissible.

References

Clavaguera F, Bolmont T, Crowther R, Abramowski D, Frank S, Probst A . Transmission and spreading of tauopathy in transgenic mouse brain. Nat Cell Biol. 2009; 11(7):909-13. PMC: 2726961. DOI: 10.1038/ncb1901. View

Villemagne V, Burnham S, Bourgeat P, Brown B, Ellis K, Salvado O . Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study. Lancet Neurol. 2013; 12(4):357-67. DOI: 10.1016/S1474-4422(13)70044-9. View

Padilla-Zambrano H, Garcia-Ballestas E, Quinones-Ossa G, Sibaja-Perez A, Agrawal A, Moscote-Salazar L . The Prion-like Properties of Amyloid-beta Peptide and Tau: Is there Any Risk of Transmitting Alzheimer's Disease During Neurosurgical Interventions?. Curr Alzheimer Res. 2020; 17(9):781-789. DOI: 10.2174/1567205017666201204164220. View

Nath A, Holtzman D, Miller B, Grinberg L, Leschek E . Insufficient evidence for an association between iatrogenic Alzheimer's disease and cadaveric pituitary-derived growth hormone. Alzheimers Dement. 2024; 20(10):7399-7402. PMC: 11485294. DOI: 10.1002/alz.14127. View

Phillips J . Why Aβ42 Is Much More Toxic than Aβ40. ACS Chem Neurosci. 2019; 10(6):2843-2847. DOI: 10.1021/acschemneuro.9b00068. View

Jaunmuktane Z, Quaegebeur A, Taipa R, Viana-Baptista M, Barbosa R, Koriath C . Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery. Acta Neuropathol. 2018; 135(5):671-679. PMC: 5904220. DOI: 10.1007/s00401-018-1822-2. View

Sabate R, Rousseau F, Schymkowitz J, Batlle C, Ventura S . Amyloids or prions? That is the question. Prion. 2015; 9(3):200-6. PMC: 4601216. DOI: 10.1080/19336896.2015.1053685. View

Fadel A, Hussain H, Hernandez R, Clichy Silva A, Estil-Las A, Hamad M . Mechanisms of Neurosyphilis-Induced Dementia: Insights into Pathophysiology. Neurol Int. 2024; 16(6):1653-1665. PMC: 11679807. DOI: 10.3390/neurolint16060120. View

Katzmarski N, Ziegler-Waldkirch S, Scheffler N, Witt C, Abou-Ajram C, Nuscher B . Aβ oligomers trigger and accelerate Aβ seeding. Brain Pathol. 2019; 30(1):36-45. PMC: 6916291. DOI: 10.1111/bpa.12734. View

10.

Rudge P, Jaunmuktane Z, Adlard P, Bjurstrom N, Caine D, Lowe J . Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years. Brain. 2015; 138(Pt 11):3386-99. PMC: 4620512. DOI: 10.1093/brain/awv235. View

11.

Jucker M, Walker L . Evidence for iatrogenic transmission of Alzheimer's disease. Nat Med. 2024; 30(2):344-345. PMC: 11492925. DOI: 10.1038/s41591-023-02768-9. View

12.

Raposo N, Planton M, Siegfried A, Calviere L, Payoux P, Albucher J . Amyloid-β transmission through cardiac surgery using cadaveric dura mater patch. J Neurol Neurosurg Psychiatry. 2020; 91(4):440-441. DOI: 10.1136/jnnp-2019-321927. View

13.

Zablocka A . [Alzheimer's disease as neurodegenerative disorder]. Postepy Hig Med Dosw (Online). 2006; 60:209-16. View

14.

Iwasaki Y, Imamura K, Iwai K, Kobayashi Y, Akagi A, Mimuro M . Autopsied case of non-plaque-type dura mater graft-associated Creutzfeldt-Jakob disease presenting with extensive amyloid-β deposition. Neuropathology. 2018; 38(5):549-556. DOI: 10.1111/neup.12503. View

15.

Takahashi R, Nagao T, Gouras G . Plaque formation and the intraneuronal accumulation of β-amyloid in Alzheimer's disease. Pathol Int. 2017; 67(4):185-193. DOI: 10.1111/pin.12520. View

16.

Marcocci M, Napoletani G, Protto V, Kolesova O, Piacentini R, Li Puma D . Herpes Simplex Virus-1 in the Brain: The Dark Side of a Sneaky Infection. Trends Microbiol. 2020; 28(10):808-820. DOI: 10.1016/j.tim.2020.03.003. View

17.

Frontzek K, Lutz M, Aguzzi A, Kovacs G, Budka H . Amyloid-β pathology and cerebral amyloid angiopathy are frequent in iatrogenic Creutzfeldt-Jakob disease after dural grafting. Swiss Med Wkly. 2016; 146:w14287. DOI: 10.4414/smw.2016.14287. View

18.

Gouras G, Almeida C, Takahashi R . Intraneuronal Abeta accumulation and origin of plaques in Alzheimer's disease. Neurobiol Aging. 2005; 26(9):1235-44. DOI: 10.1016/j.neurobiolaging.2005.05.022. View

19.

Hamaguchi T, Ono K, Yamada M . Transmission of Cerebral β-Amyloidosis Among Individuals. Neurochem Res. 2022; 47(9):2469-2477. DOI: 10.1007/s11064-022-03566-4. View

20.

Walker L, Schelle J, Jucker M . The Prion-Like Properties of Amyloid-β Assemblies: Implications for Alzheimer's Disease. Cold Spring Harb Perspect Med. 2016; 6(7). PMC: 4930920. DOI: 10.1101/cshperspect.a024398. View