Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2015;47(2):329-33.
doi: 10.3233/JAD-150065.

Reduced Incidence of Dementia in Solid Organ Transplant Patients Treated with Calcineurin Inhibitors

Giulio Taglialatela  1 , Cristiana Rastellini  2   3 , Luca Cicalese  2
Affiliations
Free PMC article

Reduced Incidence of Dementia in Solid Organ Transplant Patients Treated with Calcineurin Inhibitors

Giulio Taglialatela et al. J Alzheimers Dis. 2015.
Free PMC article

Abstract

Experimental evidence suggests that the protein phosphatase calcineurin mediates the action of amyloid-β (Aβ) oligomers, the most toxic amyloid species thought to drive initial cognitive decline in Alzheimer's disease (AD). However, there is currently no evidence that inhibition of calcineurin could prevent the onset of AD in humans. Here, we report for the first time that individuals chronically treated with calcineurin inhibitors to prevent solid organ transplant rejection have a significantly lower incidence of AD/dementia as compared to the general population. This result prompts further clinical development of calcineurin inhibition as a viable treatment for AD.

Keywords: Alzheimer’s disease; FK506; calcineurin; dementia; solid organ transplant.

PubMed Disclaimer

Figures

Fig.1
Fig.1
Prevalence of clinically diagnosed dementia (including Alzheimer’s disease) in the general population as compared to transplanted patients treated with immunosuppressive calcineurin inhibitors (CNI). Patients were grouped according to age at time of last follow up medical examination or death. Table underneath figure shows actual numbers in the transplanted patient cohort studied for the present report.  ***p <  0.0001 as compared to age-matched group in the general population (χ 2 test).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Larson ME, Lesne SE. Soluble Abeta oligomer production and toxicity. J Neurochem. 2012;120(Suppl 1):125–139. - PMC - PubMed
    1. Walsh DM, Selkoe DJ. A beta oligomers - a decade of discovery. J Neurochem. 2007;101:1172–1184. - PubMed
    1. Ma T, Klann E. Amyloid beta: Linking synaptic plasticity failure to memory disruption in Alzheimer’s disease. J Neurochem. 2012;120(Suppl 1):140–148. - PMC - PubMed
    1. Bjorklund NL, Reese LC, Sadagoparamanujam VM, Ghirardi V, Woltjer RL, Taglialatela G. Absence of amyloidbeta oligomers at the postsynapse and regulated synaptic Zn2+ in cognitively intact aged individuals withAlzheimer’s disease neuropathology. Mol Neurodegener. 2012;7:23. - PMC - PubMed
    1. Wilcox KC, Lacor PN, Pitt J, Klein WL. Abeta oligomer-induced synapse degeneration in Alzheimer’s disease. Cell Mol Neurobiol. 2011;31:939–948. - PMC - PubMed

Publication types

Substances