At a research talk earlier this year, the speaker made a somewhat offhanded comment when they said that people who get cancer usually do not develop Alzheimer’s and vice versa. The topic of the talk was neither Alzheimer’s nor cancer, so this claim was not explored much further, though it left me wondering whether this was true, and then of course, wondering which end of the stick I would end up with.
Interestingly, the speaker’s claim is supported by evidence in that population-level studies have revealed that cancer survivors do indeed have a lower risk of later developing Alzheimer’s Disease. These data, however, do not suggest that the diseases are mutually exclusive, and the magnitude of these effects widely varies by study with some reporting numbers as low as 11%, others estimating risk of Dementia (a collection of symptoms, not directly Alzheimer’s disease) lowering by 25% with a cancer diagnosis and other estimates as high as 45% reduction in risk of Alzheimer’s.
So, we know that a statistical pattern exists across populations, but what can be said of the cause of this association? Does having one disease somehow protect you from the other? Well, like most things in science, the truth lives in a gray area. From a high level, we can derive some seemingly valid reasoning: cancer is a disease characterized by excessive cell proliferation, that is cells dividing too much, whereas Alzheimer’s involves the degeneration and death of brain tissues. So, at a glance, these diseases do seem somewhat opposed to each other in function in that one kills cells and the other makes too many extra cells. This is where reality checks us though. Lung cancer for example is one type of cancer where particularly significant inverse relationships exist with Alzheimer’s incidence yet has nothing to do with brain tissue. In other words, lung cancer means mutated lung cells dividing too much, not brain cells. So why would we see less Alzheimer’s associated brain tissue death in situations where other cells are proliferating too much, yet brain tissue does not experience the same over-growth?
This is again, where we are checked by reality. The observed inverse relationship between Alzheimer’s and cancer is not as simple as ‘too much cell death + too much cell survival = normal function’, however, studies suggest that cancer and Alzheimer’s may share overlapping biological pathways that are dysregulated in different directions, making the association biologically plausible rather than purely statistical. For examples, a protein called Pin1 is implicated in both diseases, and a strong candidate for explaining the inverse relationship. In many cancers, Pin1 is over-expressed whilst in Alzheimer’s it is often down-regulated or inactivated by several mechanisms. Moreover, in Alzheimer’s, Pin1 is implicated in both major axes of the disease pathology where its absence leads to more amyloid-beta production, and tau protein hyperphosphorylations (two major hallmarks of Alzheimer’s development).
It would seem that this common mechanism is exactly what scientists are looking for in that Pin1 cannot be both up- and down-regulated at the same time, and dysregulation in either direction is (seemingly) exclusively implicated in either cancer or Alzheimer’s. However, we must leave room for nuance. Both diseases have extremely complicated pathologies that have yet to be fully understood. So, it is likely the case that other mechanisms also contribute to the inverse relationship seen in the prevalence of these diseases and remain to be fully characterized.
The most important takeaway is that this is not prophecy. Having cancer does not mean you are “safe” from Alzheimer’s, and developing Alzheimer’s does not mean cancer was somehow avoided. What researchers have found though, is a strange statistical pattern that points to something deeper. The same biological machinery that keeps cells alive, dividing, repairing, or dying may push the body toward cancer in one context and neural degeneration in another. If that is true, then the relationship between these diseases is not just a curiosity; it is a clue, and may yet help us understand how to treat each disease more effectively.
References
Abner, E. L., Karanth, S. D., Aung, K. Z., & Nelson, P. T. (2025). The inverse association between cancer and Alzheimer’s disease: Evidence from neuropathological studies. Alzheimer’s & Dementia, 20(Suppl. 6), e087469. https://doi.org/10.1002/alz.087469
Bassil, D. T., Zheng, B., Su, B., Kafetsouli, D., Udeh-Momoh, C., Tzoulaki, I., Ahmadi-Abhari, S., Muller, D. C., Riboli, E., & Middleton, L. T. (2024). Lower incidence of dementia following cancer diagnoses: Evidence from a large cohort and Mendelian randomization study. The Journal of Prevention of Alzheimer’s Disease, 11(5), 1397-1405. https://doi.org/10.14283/jpad.2024.135
Behrens, M. I., Lendon, C., & Roe, C. M. (2009). A common biological mechanism in cancer and Alzheimer’s disease? Current Alzheimer Research, 6(3), 196-204. https://doi.org/10.2174/156720509788486608
Driver, J. A., Zhou, X. Z., & Lu, K. P. (2015). Pin1 dysregulation helps to explain the inverse association between cancer and Alzheimer’s disease. Biochimica et Biophysica Acta, 1850(10), 2069-2076. https://doi.org/10.1016/ j.bbagen.2014.12.025
Ospina-Romero, M., Glymour, M. M., Hayes-Larson, E., Mayeda, E. R., Graff, R. E., Brenowitz, W. D., Ackley, S. F., Witte, J. S., & Kobayashi, L. C. (2020). Association between Alzheimer disease and cancer with evaluation of study biases: A systematic review and meta-analysis. JAMA Network Open, 3(11), e2025515. https://doi.org/10.1001/jamanetworkopen.2020.25515
Shi, H.-B., Tang, B., Liu, Y.-W., Wang, X.-F., & Chen, G.-J. (2015). Alzheimer disease and cancer risk: A meta-analysis. Journal of Cancer Research and Clinical Oncology, 141(3), 485-494. https://doi.org/10.1007/s00432-014-1773-5
UniProt Consortium. (n.d.). PIN1 - Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (UniProtKB: Q13526).Retrieved March 1, 2026, from https://www.uniprot.org/uniprotkb/Q13526/entry
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