How biochemical pathways for disease may be triggered by early-life events

Debomoy Lahiri, Bryan Maloney, Nasser H. Zawia

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Alzheimer's disease (AD) is the most common form of dementia among the elderly and usually appears late in adult life. It is presently uncertain when process of this disease starts and how long these pathobiochemical processes take to develop. Therefore, we address the timing and nature of triggers that lead to AD. To explain the etiology of AD, we propose a Latent Early-life Associated Regulation (LEARn) model which postulates latent expression of specific genes triggered at the developmental stage of life. This model integrates both the neuropathological features (e.g., amyloid-loaded plaques and tau-laden tangles) and environmental conditions (e.g., diet, metal exposure, and hormones) associated with AD. In the LEARn model, environmental agents could perturb gene regulation in a long-term fashion, beginning at early developmental stages, but these perturbations would not have pathological results until significantly later in life. The LEARn model operates through the regulatory region (promoter) of the gene, specifically through changes in methylation and oxidation status within the promoter of specific genes. The LEARn model combines genetic and environmental risk factors to explain the etiology of the most common, sporadic, form of AD.

Original languageEnglish
Title of host publicationCurrent Hypotheses and Research Milestones in Alzheimer's Disease
PublisherSpringer US
Pages205-214
Number of pages10
ISBN (Print)9780387879949
DOIs
StatePublished - 2009

Fingerprint

Alzheimer Disease
Genes
Nucleic Acid Regulatory Sequences
Genetic Models
Amyloid Plaques
Methylation
Dementia
Metals
Hormones
Diet
Gene Expression

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Lahiri, D., Maloney, B., & Zawia, N. H. (2009). How biochemical pathways for disease may be triggered by early-life events. In Current Hypotheses and Research Milestones in Alzheimer's Disease (pp. 205-214). Springer US. https://doi.org/10.1007/978-0-387-87995-6_17

How biochemical pathways for disease may be triggered by early-life events. / Lahiri, Debomoy; Maloney, Bryan; Zawia, Nasser H.

Current Hypotheses and Research Milestones in Alzheimer's Disease. Springer US, 2009. p. 205-214.

Research output: Chapter in Book/Report/Conference proceedingChapter

Lahiri, D, Maloney, B & Zawia, NH 2009, How biochemical pathways for disease may be triggered by early-life events. in Current Hypotheses and Research Milestones in Alzheimer's Disease. Springer US, pp. 205-214. https://doi.org/10.1007/978-0-387-87995-6_17
Lahiri D, Maloney B, Zawia NH. How biochemical pathways for disease may be triggered by early-life events. In Current Hypotheses and Research Milestones in Alzheimer's Disease. Springer US. 2009. p. 205-214 https://doi.org/10.1007/978-0-387-87995-6_17
Lahiri, Debomoy ; Maloney, Bryan ; Zawia, Nasser H. / How biochemical pathways for disease may be triggered by early-life events. Current Hypotheses and Research Milestones in Alzheimer's Disease. Springer US, 2009. pp. 205-214
@inbook{67278396bf7745da8637925ce7dd94bb,
title = "How biochemical pathways for disease may be triggered by early-life events",
abstract = "Alzheimer's disease (AD) is the most common form of dementia among the elderly and usually appears late in adult life. It is presently uncertain when process of this disease starts and how long these pathobiochemical processes take to develop. Therefore, we address the timing and nature of triggers that lead to AD. To explain the etiology of AD, we propose a Latent Early-life Associated Regulation (LEARn) model which postulates latent expression of specific genes triggered at the developmental stage of life. This model integrates both the neuropathological features (e.g., amyloid-loaded plaques and tau-laden tangles) and environmental conditions (e.g., diet, metal exposure, and hormones) associated with AD. In the LEARn model, environmental agents could perturb gene regulation in a long-term fashion, beginning at early developmental stages, but these perturbations would not have pathological results until significantly later in life. The LEARn model operates through the regulatory region (promoter) of the gene, specifically through changes in methylation and oxidation status within the promoter of specific genes. The LEARn model combines genetic and environmental risk factors to explain the etiology of the most common, sporadic, form of AD.",
author = "Debomoy Lahiri and Bryan Maloney and Zawia, {Nasser H.}",
year = "2009",
doi = "10.1007/978-0-387-87995-6_17",
language = "English",
isbn = "9780387879949",
pages = "205--214",
booktitle = "Current Hypotheses and Research Milestones in Alzheimer's Disease",
publisher = "Springer US",

}

TY - CHAP

T1 - How biochemical pathways for disease may be triggered by early-life events

AU - Lahiri, Debomoy

AU - Maloney, Bryan

AU - Zawia, Nasser H.

PY - 2009

Y1 - 2009

N2 - Alzheimer's disease (AD) is the most common form of dementia among the elderly and usually appears late in adult life. It is presently uncertain when process of this disease starts and how long these pathobiochemical processes take to develop. Therefore, we address the timing and nature of triggers that lead to AD. To explain the etiology of AD, we propose a Latent Early-life Associated Regulation (LEARn) model which postulates latent expression of specific genes triggered at the developmental stage of life. This model integrates both the neuropathological features (e.g., amyloid-loaded plaques and tau-laden tangles) and environmental conditions (e.g., diet, metal exposure, and hormones) associated with AD. In the LEARn model, environmental agents could perturb gene regulation in a long-term fashion, beginning at early developmental stages, but these perturbations would not have pathological results until significantly later in life. The LEARn model operates through the regulatory region (promoter) of the gene, specifically through changes in methylation and oxidation status within the promoter of specific genes. The LEARn model combines genetic and environmental risk factors to explain the etiology of the most common, sporadic, form of AD.

AB - Alzheimer's disease (AD) is the most common form of dementia among the elderly and usually appears late in adult life. It is presently uncertain when process of this disease starts and how long these pathobiochemical processes take to develop. Therefore, we address the timing and nature of triggers that lead to AD. To explain the etiology of AD, we propose a Latent Early-life Associated Regulation (LEARn) model which postulates latent expression of specific genes triggered at the developmental stage of life. This model integrates both the neuropathological features (e.g., amyloid-loaded plaques and tau-laden tangles) and environmental conditions (e.g., diet, metal exposure, and hormones) associated with AD. In the LEARn model, environmental agents could perturb gene regulation in a long-term fashion, beginning at early developmental stages, but these perturbations would not have pathological results until significantly later in life. The LEARn model operates through the regulatory region (promoter) of the gene, specifically through changes in methylation and oxidation status within the promoter of specific genes. The LEARn model combines genetic and environmental risk factors to explain the etiology of the most common, sporadic, form of AD.

UR - http://www.scopus.com/inward/record.url?scp=84900062590&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84900062590&partnerID=8YFLogxK

U2 - 10.1007/978-0-387-87995-6_17

DO - 10.1007/978-0-387-87995-6_17

M3 - Chapter

SN - 9780387879949

SP - 205

EP - 214

BT - Current Hypotheses and Research Milestones in Alzheimer's Disease

PB - Springer US

ER -