Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Perspective
  • Published:

The advent of Alzheimer treatments will change the trajectory of human aging

Abstract

Slowing neurodegenerative disorders of late life has lagged behind progress on other chronic diseases. But advances in two areas, biochemical pathology and human genetics, have now identified early pathogenic events, enabling molecular hypotheses and disease-modifying treatments. A salient example is the discovery that antibodies to amyloid ß-protein, long debated as a causative factor in Alzheimer’s disease (AD), clear amyloid plaques, decrease levels of abnormal tau proteins and slow cognitive decline. Approval of amyloid antibodies as the first disease-modifying treatments means a gradually rising fraction of the world’s estimated 60 million people with symptomatic disease may decline less or even stabilize. Society is entering an era in which the unchecked devastation of AD is no longer inevitable. This Perspective considers the impact of slowing AD and other neurodegenerative disorders on the trajectory of aging, allowing people to survive into late life with less functional decline. The implications of this moment for medicine and society are profound.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Key milestones in AD research.
Fig. 2: A summary of Alzheimer’s disease pathobiology and therapeutic targets.

Similar content being viewed by others

References

  1. Kang, J. et al. The precursor of Alzheimer’s disease amyloid A4 protein resembles a cell-surface receptor. Nature 325, 733–736 (1987).

    Article  CAS  PubMed  Google Scholar 

  2. Wasco, W. et al. Identification of a mouse brain cDNA that encodes a protein related to the Alzheimer disease-associated amyloid β protein precursor. Proc. Natl Acad. Sci. USA 89, 10758–10762 (1992).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Wasco, W. et al. Isolation and characterization of APLP2 encoding a homologue of the Alzheimer’s associated amyloid β protein precursor. Nat. Genet. 5, 95–100 (1993).

    Article  CAS  PubMed  Google Scholar 

  4. Sherrington, R. et al. Cloning of a novel gene bearing missense mutations in early onset familial Alzheimer disease. Nature 375, 754–760 (1995).

    Article  CAS  PubMed  Google Scholar 

  5. Rogaev, E. I. et al. Familial Alzheimer’s disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer’s disease type 3 gene. Nature 376, 775–778 (1995).

    Article  CAS  PubMed  Google Scholar 

  6. Vassar, R. et al. Beta-secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE. Science 286, 735–741 (1999).

    Article  CAS  PubMed  Google Scholar 

  7. Sinha, S. et al. Purification and cloning of amyloid precursor protein beta-secretase from human brain. Nature 402, 537–540 (1999).

    Article  CAS  PubMed  Google Scholar 

  8. Ghosh, A. K. et al. Design of potent inhibitors for human brain memapsin 2 (beta-secretase). J. Am. Chem. Soc. 122, 3522–3523 (2000).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Wolfe, M. S. et al. Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity. Nature 398, 513–517 (1999).

    Article  CAS  PubMed  Google Scholar 

  10. Struhl, G. & Greenwald, I. Presenilin is required for activity and nuclear access of Notch in Drosophila. Nature 398, 522–525 (1999).

    Article  CAS  PubMed  Google Scholar 

  11. De Strooper, B. et al. A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain. Nature 398, 518–522 (1999).

    Article  PubMed  Google Scholar 

  12. Katzman, R. Editorial: the prevalence and malignancy of Alzheimer disease. A major killer. Arch. Neurol. 33, 217–218 (1976).

    Article  CAS  PubMed  Google Scholar 

  13. Martens, Y. A. et al. ApoE cascade hypothesis in the pathogenesis of Alzheimer’s disease and related dementias. Neuron 110, 1304–1317 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Knopman, D. S. et al. Alzheimer disease. Nat. Rev. Dis. Prim. 7, 33 (2021).

    Article  PubMed  Google Scholar 

  15. Chen, X. & Holtzman, D. M. Emerging roles of innate and adaptive immunity in Alzheimer’s disease. Immunity 55, 2236–2254 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Alzheimer, A. Ueber eine eigenartige Erkrankung der Hirnrinde. Centralblatt Nervenheilkd. Psychiatr. 30, 177–179 (1907).

    Google Scholar 

  17. Davies, P. & Maloney, A. J. Selective loss of central cholinergic neurons in Alzheimer’s disease. Lancet 2, 1403 (1976).

    Article  CAS  PubMed  Google Scholar 

  18. White, P. et al. Neocortical cholinergic neurons in elderly people. Lancet 1, 668–671 (1977).

    Article  CAS  PubMed  Google Scholar 

  19. Glenner, G. G. & Wong, C. W. Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem. Biophys. Res. Commun. 120, 885–890 (1984).

    Article  CAS  PubMed  Google Scholar 

  20. Glenner, G. G. & Wong, C. W. Alzheimer’s disease and Down’s syndrome: sharing of a unique cerebrovascular amyloid fibril protein. Biochem. Biophys. Res. Commun. 122, 1131–1135 (1984).

    Article  CAS  PubMed  Google Scholar 

  21. Masters, C. L. et al. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc. Natl Acad. Sci. USA 82, 4245–4249 (1985).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Levy, E. et al. Mutation of the Alzheimer’s disease amyloid gene in hereditary cerebral hemorrhage, Dutch-type. Science 248, 1124–1126 (1990).

    Article  CAS  PubMed  Google Scholar 

  23. Goate, A. et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer’s disease. Nature 349, 704–706 (1991).

    Article  CAS  PubMed  Google Scholar 

  24. Haass, C. et al. Amyloid β-peptide is produced by cultured cells during normal metabolism. Nature 359, 322–325 (1992).

    Article  CAS  PubMed  Google Scholar 

  25. Games, D. et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature 373, 523–527 (1995).

    Article  CAS  PubMed  Google Scholar 

  26. Brion, J., Passareiro, E., Nunez, J. & Flament-Durand, J. Mise en evidence immunologique de la protein tau au niveau des lesions de degenerescence neurofibrillaire de la maladie d’Alzheimer. Arch. Biol. 95, 229–235 (1985).

    Google Scholar 

  27. Nukina, N. & Ihara, Y. One of the antigenic determinants of paired helical filaments is related to tau protein. J. Biochem. 99, 1541–1544 (1986).

    Article  CAS  PubMed  Google Scholar 

  28. Kosik, K. S., Joachim, C. L. & Selkoe, D. J. Microtubule-associated protein, tau, is a major antigenic component of paired helical filaments in Alzheimer’s disease. Proc. Natl Acad. Sci. USA 83, 4044–4048 (1986).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Grundke-Iqbal, I. et al. Abnormal phosphorylation of the microtubule-associated protein t (tau) in Alzheimer cytoskeletal pathology. Proc. Natl Acad. Sci. USA 83, 4913–4917 (1986).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Hutton, M. et al. Association of missense and 5′-splice-site mutations in tau with the inherited FTDP-17. Nature 393, 702–705 (1998).

    Article  CAS  PubMed  Google Scholar 

  31. Strittmatter, W. J. et al. Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proc. Natl Acad. Sci. USA 90, 1977–1981 (1993).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Selkoe, D. J. Preventing Alzheimer’s disease. Science 337, 1488–1492 (2012).

    Article  CAS  PubMed  Google Scholar 

  33. Jonsson, T. et al. A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline. Nature 488, 96–99 (2012).

    Article  CAS  PubMed  Google Scholar 

  34. Prasher, V. P. et al. Molecular mapping of Alzheimer-type dementia in Down’s syndrome. Ann. Neurol. 43, 380–383 (1998).

    Article  CAS  PubMed  Google Scholar 

  35. Lemere, C. A. et al. Sequence of deposition of heterogeneous amyloid β-peptides and Apo E in Down syndrome: implications for initial events in amyloid plaque formation. Neurobiol. Dis. 3, 16–32 (1996).

    Article  CAS  PubMed  Google Scholar 

  36. Mann, D. M. & Iwatsubo, T. Diffuse plaques in the cerebellum and corpus striatum in Down’s syndrome contain amyloid beta protein (Aβ) only in the form of Aβ42(43). Neurodegeneration 5, 115–120 (1996).

    Article  CAS  PubMed  Google Scholar 

  37. Rovelet-Lecrux, A. et al. APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy. Nat. Genet. 38, 24–26 (2006).

    Article  CAS  PubMed  Google Scholar 

  38. Corder, E. H. et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science 261, 921–923 (1993).

    Article  CAS  PubMed  Google Scholar 

  39. Castellano, J. M. et al. Human apoE isoforms differentially regulate brain amyloid-β peptide clearance. Sci. Transl. Med. 3, 89ra57 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Zhang, Q. et al. Risk prediction of late-onset Alzheimer’s disease implies an oligogenic architecture. Nat. Commun. 11, 4799 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Wightman, D. P. et al. A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease. Nat. Genet. 53, 1276–1282 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Kakuda, N. et al. γ-Secretase activity is associated with braak senile plaque stages. Am. J. Pathol. 190, 1323–1331 (2020).

    Article  CAS  PubMed  Google Scholar 

  43. Kakuda, N. et al. Altered gamma-secretase activity in mild cognitive impairment and Alzheimer’s disease. EMBO Mol. Med. 4, 344–352 (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Huang, Z. et al. Proteomics of resilience to Alzheimer’s disease identifies brain regional soluble Aβ levels, actin filament processes, and response to injury. Preprint at bioRxiv https://doi.org/10.1101/2022.10.09.511430 (2022).

  45. Glenner, G. G. Amyloid deposits and amyloidosis: the beta-fibrilloses (first of two parts). N. Engl. J. Med. 302, 1283–1292 (1980).

    Article  CAS  PubMed  Google Scholar 

  46. Selkoe, D. J. The molecular pathology of Alzheimer’s disease. Neuron 6, 487–498 (1991).

    Article  CAS  PubMed  Google Scholar 

  47. Hardy, J. A. & Higgins, G. A. Alzheimer’s disease: the amyloid cascade hypothesis. Science 256, 184–185 (1992).

    Article  CAS  PubMed  Google Scholar 

  48. Karran, E. & De Strooper, B. The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics. Nat. Rev. Drug Discov. 21, 306–318 (2022).

    Article  CAS  PubMed  Google Scholar 

  49. Haass, C. & Selkoe, D. If amyloid drives Alzheimer disease, why have anti-amyloid therapies not yet slowed cognitive decline? PLoS Biol. 20, e3001694 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  50. Schenk, D. et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 400, 173–177 (1999).

    Article  CAS  PubMed  Google Scholar 

  51. Bard, F. et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nat. Med. 6, 916–919 (2000).

    Article  CAS  PubMed  Google Scholar 

  52. Monsonego, A. et al. Increased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease. J. Clin. Invest. 112, 415–422 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  53. Serrano-Pozo, A. et al. Beneficial effect of human anti-amyloid-β active immunization on neurite morphology and tau pathology. Brain 133, 1312–1327 (2010).

    Article  PubMed  PubMed Central  Google Scholar 

  54. Sevigny, J. et al. The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease. Nature 537, 50–56 (2016).

    Article  CAS  PubMed  Google Scholar 

  55. Lord, A. et al. An amyloid-β protofibril-selective antibody prevents amyloid formation in a mouse model of Alzheimer’s disease. Neurobiol. Dis. 36, 425–434 (2009).

    Article  CAS  PubMed  Google Scholar 

  56. Salloway, S. et al. A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate Alzheimer disease. Neurology 73, 2061–2070 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Sperling, R. A. et al. Trial of solanezumab in preclinical Alzheimer’s disease. N. Engl. J. Med. 389, 1096–1107 (2023).

  58. Budd Haeberlein, S. et al. Two randomized phase 3 studies of aducanumab in early Alzheimer’s disease. J. Prev. Alzheimers Dis. 9, 197–210 (2022).

    CAS  PubMed  Google Scholar 

  59. van Dyck, C. H. et al. Lecanemab in early Alzheimer’s disease. N. Engl. J. Med. 388, 9–21 (2023).

    Article  PubMed  Google Scholar 

  60. Sims, J. R. et al. Donanemab in early symptomatic Alzheimer Disease: the TRAILBLAZER-ALZ 2 randomized clinical trial. JAMA 330, 512–527 (2023).

  61. Johnson, K. et al. Biomarker assessments from Clarity AD: downstream implications of targeting protofibrils and tau as a predictive biomarker. In 16th Clinical Trialson Alzheimer’s Disease (ed. Shobha, D.) S9–S10 (CTAD, 2023).

  62. Rafii, M. S. et al. The AHEAD 3-45 Study: design of a prevention trial for Alzheimer’s disease. Alzheimers Dement. 19, 1227–1233 (2023).

    Article  CAS  PubMed  Google Scholar 

  63. Boxer, A. L. & Sperling, R. Accelerating Alzheimer’s therapeutic development: the past and future of clinical trials. Cell 186, 4757–4772 (2023).

    Article  CAS  PubMed  Google Scholar 

  64. Cummings, J. et al. Lecanemab: appropriate use recommendations. J. Prev. Alzheimers Dis. 10, 362–377 (2023).

    CAS  PubMed  PubMed Central  Google Scholar 

  65. Rosenberg, A., Mangialasche, F., Ngandu, T., Solomon, A. & Kivipelto, M. Multidomain interventions to prevent cognitive impairment, Alzheimer’s disease, and dementia: from FINGER to world-wide FINGERS. J. Prev. Alzheimers Dis. 7, 29–36 (2020).

    CAS  PubMed  Google Scholar 

  66. Weggen, S. et al. A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity. Nature 414, 212–216 (2001).

    Article  CAS  PubMed  Google Scholar 

  67. Ohki, Y. et al. Phenylpiperidine-type gamma-secretase modulators target the transmembrane domain 1 of presenilin 1. EMBO J. 30, 4815–4824 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  68. Crump, C. J., Johnson, D. S. & Li, Y. M. Development and mechanism of γ-secretase modulators for Alzheimer’s disease. Biochemistry 52, 3197–3216 (2013).

  69. Wagner, S. L. et al. Soluble γ-secretase modulators selectively inhibit the production of the 42-amino acid amyloid beta peptide variant and augment the production of multiple carboxy-truncated amyloid beta species. Biochemistry 53, 702–713 (2014).

    Article  CAS  PubMed  Google Scholar 

  70. Johnson, D. S., Li, Y.-M., Pettersson, M. & St George-Hyslop, P. H. Structural and chemical biology of presenilin complexes. Cold Spring Harb. Perspect. Med. 7, a024067 (2017).

  71. Liu, L., Lauro, B. M., Wolfe, M. S. & Selkoe, D. J. Hydrophilic loop 1 of presenilin-1 and the APP GxxxG transmembrane motif regulate gamma-secretase function in generating Alzheimer-causing Abeta peptides. J. Biol. Chem. 296, 100393 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  72. McGowan, E. et al. Aβ42 is essential for parenchymal and vascular amyloid deposition in mice. Neuron 47, 191–199 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Kim, J. et al. Aβ40 inhibits amyloid deposition in vivo. J. Neurosci. 27, 627–633 (2007).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  74. Sturm, S. RG6289, A new γ-secretase modulator for the treatment of alzheimer’s disease: results from a phase I healthy volunteer study. In 16th Clinical Trials on Alzheimers Disease (ed. Shobha, D.) S23-24 (CTAD, 2023).

  75. Rynearson, K. D. et al. Preclinical validation of a potent γ-secretase modulator for Alzheimer’s disease prevention. J. Exp. Med. 218, e20202560 (2021).

  76. Edwards, A. L. et al. Exploratory tau biomarker results from a multiple ascending-dose study of BIIB080 in Alzheimer disease: a randomized clinical trial. JAMA Neurol. 80, 1344–1352 (2023).

  77. Frenkel, D. et al. A nasal proteosome adjuvant activates microglia and prevents amyloid deposition. Ann. Neurol. 63, 591–601 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  78. He, W. G. D. & Kowal, P. U.S. Census Bureau, International Population Reports P95/16-1, An Aging World: 2015 (US Government Publishing Office, 2016).

  79. US Census Bureau. 2014 National Population Projections: Downloadable Files (2014).

  80. Rajan, K. B. et al. Population estimate of people with clinical Alzheimer’s disease and mild cognitive impairment in the United States (2020–2060). Alzheimers Dement. 17, 1966–1975 (2021).

    Article  PubMed  Google Scholar 

  81. Yaffe, K. et al. Effect of socioeconomic disparities on incidence of dementia among biracial older adults: prospective study. Br. Med. J. 347, f7051 (2013).

    Article  Google Scholar 

  82. Plassman, B. L. et al. Prevalence of dementia in the United States: the aging, demographics, and memory study. Neuroepidemiology 29, 125–132 (2007).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Alzheimer’s Association. Alzheimer’s Disease Facts and Figures 2024 (Alzheimer’s Association, 2024).

  84. CDC WONDER Online Database: About Underlying Cause of Death, 1999–2020 (US Centers for Disease Control, accessed 9 December 2022).

  85. US Burden of Disease Collaborators Collaborators et al. The state of US health, 1990–2016: burden of diseases, injuries, and risk factors among US states. JAMA 319, 1444–1472 (2018).

    Article  Google Scholar 

  86. Brunnstrom, H. R. & Englund, E. M. Cause of death in patients with dementia disorders. Eur. J. Neurol. 16, 488–492 (2009).

    Article  CAS  PubMed  Google Scholar 

  87. Arrighi, H. M., Neumann, P. J., Lieberburg, I. M. & Townsend, R. J. Lethality of Alzheimer disease and its impact on nursing home placement. Alzheimer Dis. Assoc. Disord. 24, 90–95 (2010).

    Article  PubMed  Google Scholar 

  88. Tejada-Vera, B. Mortality from Alzheimer’s disease in the United States: data for 2000 and 2010. NCHS Data Brief 1–8 (2013).

  89. Schrijvers, E. M. et al. Is dementia incidence declining?: trends in dementia incidence since 1990 in the Rotterdam Study. Neurology 78, 1456–1463 (2012).

    Article  CAS  PubMed  Google Scholar 

  90. Alzheimer’s Association. Changing the Trajectory of Alzheimer’s Disease: How a Treatment by 2025 Saves Lives and Dollars (Alzheimer’s Association, 2015).

  91. Zissimopoulos, J., Crimmins, E. & St Clair, P. The value of delaying Alzheimer’s disease onset. Forum Health Econ. Policy 18, 25–39 (2014).

    Article  PubMed  PubMed Central  Google Scholar 

  92. Alzheimer’s Association. 2024 Alzheimers Disease Facts and Figures (Alzheimer’s Association, 2024).

  93. Hall, K. S. et al. Prevalence rates for dementia and Alzheimer’s disease in African Americans: 1992 versus 2001. Alzheimers Dement. 5, 227–233 (2009).

    Article  PubMed  Google Scholar 

  94. Dufour, A. B., Shaffer, M. L., D’Agata, E. M., Habtemariam, D. & Mitchell, S. L. Survival after suspected urinary tract infection in individuals with advanced dementia. J. Am. Geriatr. Soc. 63, 2472–2477 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  95. Nicolle, L. E. Urinary tract infection in long-term-care facility residents. Clin. Infect. Dis. 31, 757–761 (2000).

    Article  CAS  PubMed  Google Scholar 

  96. Lin, P. J., Fillit, H. M., Cohen, J. T. & Neumann, P. J. Potentially avoidable hospitalizations among Medicare beneficiaries with Alzheimer’s disease and related disorders. Alzheimers Dement. 9, 30–38 (2013).

    Article  PubMed  Google Scholar 

  97. Skaria, A. P. The economic and societal burden of Alzheimer disease: managed care considerations. Am. J. Manag. Care 28, S188–S196 (2022).

    Article  PubMed  Google Scholar 

  98. Albert, S. M. et al. Hospitalization and Alzheimer’s disease: results from a community-based study. J. Gerontol. A Biol. Sci. Med Sci. 54, M267–M271 (1999).

    Article  CAS  PubMed  Google Scholar 

  99. Fillit, H., Hill, J. W. & Futterman, R. Health care utilization and costs of Alzheimer’s disease: the role of co-morbid conditions, disease stage, and pharmacotherapy. Fam. Med. 34, 528–535 (2002).

    PubMed  Google Scholar 

  100. Fanning, S. et al. Lipidomic analysis of α-synuclein neurotoxicity identifies stearoyl CoA desaturase as a target for parkinson treatment. Mol. Cell. 73, 1001–1014(2019).

    Article  CAS  PubMed  Google Scholar 

  101. Nuber, S. et al. A stearoyl-coenzyme a dDesaturase inhibitor prevents multiple Parkinson disease phenotypes in α-synuclein mice. Ann. Neurol. 89, 74–90 (2021).

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Contributions

D.J.S. is the only contributor to the piece.

Corresponding author

Correspondence to Dennis J. Selkoe.

Ethics declarations

Competing interests

D.J.S. is a director of and consultant to Prothena Biosciences and an ad hoc consultant to Eisai.

Peer review

Peer review information

Nature Aging thanks Wiesje van der Flier, Todd Golde, and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Selkoe, D.J. The advent of Alzheimer treatments will change the trajectory of human aging. Nat Aging 4, 453–463 (2024). https://doi.org/10.1038/s43587-024-00611-5

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s43587-024-00611-5

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing