ReviewFrontiers in cell and developmental biology2022
Early-Life Environment Influence on Late-Onset Alzheimer's Disease.
Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.The EMBO journal · 2026Article
- Features of Alteration in MAPK Pathway Activity in the Postnatal Brain of a Rat Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Are neurodegenerative diseases late-onset neurodevelopmental disorders? Tracing the developmental origins of neuronal vulnerability.Frontiers in neuroscience · 2026Review
- Impact of prenatal environmental exposure on offspring neurodevelopment and susceptibility to neurodegenerative diseases: mechanisms and perspectives.Frontiers in public health · 2026Review
- Metabolome informs about the chemical exposome and links to brain health.Environment international · 2025Review
- Sequential emergence and contraction of epithelial subtypes in the prenatal human choroid plexus revealed by a stem cell model.Nature communications · 2025Article
- Rethinking Depression-Beyond Neurotransmitters: An Integrated Psychoneuroendocrineimmunology Framework for Depression's Pathophysiology and Tailored Treatment.International journal of molecular sciences · 2025Review
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- Predicting cellular adaptation proteins dependent on eIF2α regulation under stress conditions: Physiological and pathophysiological implications in neuronal function.Computational and structural biotechnology journal · 2025Article
- Exosomal MicroRNAs in Alzheimer's Disease: Unveiling Their Role and Pioneering Tools for Diagnosis and Treatment.Journal of clinical medicine · 2024Review
- Exposure to Metals, Pesticides, and Air Pollutants: Focus on Resulting DNA Methylation Changes in Neurodegenerative Diseases.Biomolecules · 2024Review
- Association of birthweight and risk of incident dementia: a prospective cohort study.GeroScience · 2024Article
- DNA methylation of imprint control regions associated with Alzheimer's disease in non-Hispanic Blacks and non-Hispanic Whites.Clinical epigenetics · 2024Article
- Consensus Paper: Cerebellum and Ageing.Cerebellum (London, England) · 2024Review
- Nasal lymphatic obstruction of CSF drainage as a possible cause of Alzheimer's disease and dementia.Frontiers in aging neuroscience · 2024Article
- Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis.Redox report : communications in free radical research · 2023Review
- Perinatal S-Adenosylmethionine Supplementation RepressesInternational journal of molecular sciences · 2023Article
- Metals in Alzheimer's Disease.Biomedicines · 2023Review
- The Rat Brain Transcriptome: From Infancy to Aging and Sporadic Alzheimer's Disease-like Pathology.International journal of molecular sciences · 2023Article
- Gene-environment interactions in Alzheimer disease: the emerging role of epigenetics.Nature reviews. Neurology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With the expand of the population's average age, the incidence of neurodegenerative disorders has dramatically increased over the last decades. Alzheimer disease (AD) which is the most prevalent neurodegenerative disease is mostly sporadic and primarily characterized by cognitive deficits and neuropathological lesions such as amyloid -β (Aβ) plaques and neurofibrillary tangles composed of hyper- and/or abnormally phosphorylated Tau protein. AD is considered a complex disease that arises from the interaction between environmental and genetic factors, modulated by epigenetic mechanisms. Besides the well-described cognitive decline, AD patients also exhibit metabolic impairments. Metabolic and cognitive perturbations are indeed frequently observed in the Developmental Origin of Health and Diseases (DOHaD) field of research which proposes that environmental perturbations during the perinatal period determine the susceptibility to pathological conditions later in life. In this review, we explored the potential influence of early environmental exposure to risk factors (maternal stress, malnutrition, xenobiotics, chemical factors … ) and the involvement of epigenetic mechanisms on the programming of late-onset AD. Animal models indicate that offspring exposed to early-life stress during gestation and/or lactation increase both AD lesions, lead to defects in synaptic plasticity and finally to cognitive impairments. This long-lasting epigenetic programming could be modulated by factors such as nutriceuticals, epigenetic modifiers or psychosocial behaviour, offering thus future therapeutic opportunity to protect from AD development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.