Bach1 Overexpression in Down Syndrome Correlates with the Alteration of the HO-1/BVR-A System: Insights for Transition to Alzheimer's Disease
Open accessAbstract
Bach1, among the genes encoded on chromosome 21, is a transcription repressor, which binds to antioxidant response elements of DNA thus inhibiting the transcription of specific genes involved in the cell stress response including heme oxygenase-1 (HO-1). HO-1 and its partner, biliverdin reductase-A (BVR-A), are upregulated in response to oxidative stress in order to protect cells against further damage. Since oxidative stress is an early event in Down syndrome (DS) and might contribute to the development of multiple deleterious DS phenotypes, including Alzheimer's disease (AD) pathology, we investigated the status of the Bach1/HO-1/BVR-A axis in DS and its possible implications for the development of AD. In the present study, we showed increased total Bach1 protein levels in the brain of all DS cases coupled with reduced induction of brain HO-1. Furthermore, increased oxidative stress could, on one hand, overcome the inhibitory effects of Bach1 and, on the other hand, promote BVR-A impairment. Our data show that the development of AD in DS subjects is characterized by (i) increased Bach1 total and poly-ubiquitination; (ii) increased HO-1 protein levels; and (iii) increased nitration of BVR-A followed by reduced activity. To corroborate our findings, we analyzed Bach1, HO-1, and BVR-A status in the Ts65Dn mouse model at 3 (young) and 15 (old) months of age. The above data support the hypothesis that the dysregulation of HO-1/BVR-A system contributes to the early increase of oxidative stress in DS and provide potential mechanistic paths involved in the neurodegenerative process and AD development.
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Both a dose effect from APP triplication and gene-environment interactions likely contribute to Alzheimer-like dementia in Down syndrome.
“It is likely that both a dose effect of triplication of APP and gene-environment interactions play a role59,60.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [60]
The Introduction (page unavailable) identifies APP as a chromosome 21 gene and reports that amyloid accumulation in Down syndrome increases with age, leading generally to Alzheimer pathology. It also says Down syndrome phenotypes need not arise exclusively from specific chromosome 21 genes. The paper does not specifically attribute Alzheimer-like dementia to an APP triplication dose effect or to gene–environment interactions. (LLM, conf=0.76)
Experimental — accuracy not yet measuredPeople with Down syndrome often develop Alzheimer-like dementia at approximately 40 to 50 years of age.
“One striking characteristic of people with DS is that at approximately 40–50 years of age, AD-like dementia often appears59,60.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [60]
The Introduction (page unavailable) says Alzheimer disease pathology generally develops in people with Down syndrome by the fourth decade of life, and Methods > Subjects says all studied cases with both Down syndrome and neuropathological Alzheimer disease were over 40. Neither passage establishes that clinical dementia often appears at ages 40–50; pathology and dementia are not interchangeable. (LLM, conf=0.85)
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Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2
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Self-citationDissecting Alzheimer disease in Down syndrome using mouse models
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The Impact of Oxidative Stress on Pediatrics Syndromes
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Tramutola, A., Pupo, G., Di Domenico, F., Barone, E., Arena, A., Lanzillotta, C., Broekaart, D., Blarzino, C., Head, E., Butterfield, D. A., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-151105 · Cited by 40 · see citing works
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Self-citationStriking a NRF2: The Rusty and Rancid Vulnerabilities Toward Ferroptosis in Alzheimer's Disease
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Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules
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Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials
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The Dysregulation of OGT/OGA Cycle Mediates Tau and APP Neuropathology in Down Syndrome
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The amplification of CNS damage in Alzheimer's disease due to SARS-CoV2 infection
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Self-citationAging, NRF2, and TAU: A Perfect Match for Neurodegeneration?
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CAPE and its synthetic derivative VP961 restore BACH1/NRF2 axis in Down Syndrome
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Self-citationOxidative Stress in Down and Williams-Beuren Syndromes: An Overview
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The Heme Oxygenase/Biliverdin Reductase System and Its Genetic Variants in Physiology and Diseases
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Redox imbalance and metabolic defects in the context of Alzheimer disease
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Self-citationAge-related alteration in HNE elimination enzymes
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Self-citationLanzillotta, C., Rataj-Baniowska, M., Prestia, F., Sette, C., Nalesso, V., Marzia Perluigi, A., Barone, E., Duchon, A., Tramutola, A., Hérault, Y., et al. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106523 · Cited by 18 · see citing works
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Loss of DNA polymerase β induces cellular senescence
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The brain heme oxygenase/biliverdin reductase system as a target in drug research and development
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Self-citationAutophagy is a promising process for linking inflammation and redox homeostasis in Down syndrome
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Advances in Research on Down Syndrome
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Intricacies of aging and Down syndrome
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Thorwald, M. A., Godoy-Lugo, J. A., Kerstiens, E., Garcia, G., Kim, M., Shemtov, S. J., Silva, J. A., Durra, S., O’Day, P. A., Mack, W. J., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70322 · Cited by 6 · see citing works
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Self-citationMitochondrial Abnormalities in Down Syndrome: Pathogenesis, Effects and Therapeutic Approaches
Izzo, A., Mollo, N., Cicatiello, R., Genesio, R., Paladino, S., Conti, A. M. F., & Nitsch, L. (2018) · InTech eBooks · doi:10.5772/intechopen.71059 · Cited by 3 · see citing works
Aging exacerbates oxidative stress and liver fibrosis in an animal model of Down Syndrome
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Self-citationWelham, A., Chorvinsky, E. A., Bhattacharya, S., Salka, K., Bera, B. S., Admasu, W., Straker, M. C., Gutierrez, M. J., Jaiswal, J. K., & Niño, G. (2025) · Frontiers in Pediatrics · doi:10.3389/fped.2025.1553571 · Cited by 2 · see citing works
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Self-citationHPPE Activates NRF2 Signaling by Liberating Heavy Metal Stores
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Down syndrome: the prevalence of Alzheimer’s disease and the role of thyroid hormone
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BACH1 orchestrates macrophage state transitions to coordinate regenerative inflammation
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Self-citationInvestigating The Role Of Dna Polymerase Beta In The Aging Phenotype Of Down Syndrome
Ahmed, A. A. (2016) · Human Biology
Lanzillotta, C., Rataj-Baniowska, M., Prestia, F., Sette, C., Nalesso, V., Marzia Perluigi, A., Barone, E., Duchon, A., Tramutola, A., Hérault, Y., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.01.02.573811
Self-citationBACH1/HO-1 axis dysregulation links Down syndrome to Alzheimer-like neurodegeneration
Domenico, F. D., Barone, E., & Marzia Perluigi, A. (2026) · Neurochemistry International · doi:10.1016/j.neuint.2026.106232
Self-citationOxidative Stress and Its Mitigation in Neurodegenerative Disorders
Butterfield, D. A. (2026) · Antioxidants · doi:10.3390/antiox15091190
Self-citationRole of Bach1 Transcription Factor in the Mechanisms of Cell Death
Klycheva, K., Silkina, M. O., Hushpulian, D. M., Razumovskaya, A. V., Zakharyants, A. A., Thomas, B., Kazakov, S. V., Gazaryan, I. G., & Nikulin, S. V. (2026) · Biochemistry (Moscow) · doi:10.1134/s0006297926601723
- Authors
- Di Domenico, F., Pupo, G., Mancuso, C., Barone, E., Paolini, F., Arena, A., Blarzino, C., Schmitt, F. A., Head, E., Butterfield, D. A., & Perluigi, M.
- Affiliations
- Department of Biochemical Sciences, Sapienza University of Rome, Italy
- Sapienza University of Rome (IT)
- Institute of Pharmacology, Catholic University School of Medicine, Rome, Italy
- Instituto Nazionale Tumori Regina Elena (IT)
- University of Kentucky (US)
- ORCID
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2015-02-19
- Volume
- 44
- Issue
- 4
- Pages
- 1107-1120
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC4677575
- OpenAlex
- W1539907006
- Cited by
- 75
- References
- 89
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 9 · 2023: 3 · 2022: 8 · 2021: 7 · 2020: 11 · 2019: 4 · 2018: 11 · 2017: 5 · 2016: 2 · 2015: 2
- FWCI
- 2.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- European Commission (2007–2013, FP7 2007-2013, 624341, FP7/2007)
- National Institutes of Health (FP7/2007-2013, HHSN275200900011C,, AG-05119)
- U.S. Public Health Service (#HHSN275200900011C)
- National Institute on Aging (P50 AG 16573, P30AG028383, P01AG005119, P50AG016573, P30 AG28383, AG0 5119)
- National Institute of Child Health and Human Development
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HHSN275200900011C, R01HD064993, N01-HD-90011)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- BACH1, Down syndrome
- MeSH terms
- Adolescent, Adult, Age Factors, Aged, Alzheimer Disease, Analysis of Variance, Animals, Brain, Child, Down Syndrome, Female, Gene Expression Regulation, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, Oxidative Stress, Oxidoreductases Acting on CH-CH Group Donors, Immunoprecipitation, Basic-Leucine Zipper Transcription Factors, Mice, Heme Oxygenase-1, Fanconi Anemia Complementation Group Proteins, Ubiquitination, Young Adult
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