Related Experiment Video

Updated: May 5, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

94.0K

Aluminum causes irreversible damage to the development of hippocampal neurons by regulating m6A RNA methylation

Lingling Yang1, Guangzi Qi2, Wenlian Rao3

  • 1College of Public Health and Management, Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China.

Toxicology Letters
|July 15, 2024
PubMed

Insights

Developmental aluminum exposure impairs hippocampal neurons by reducing m6A RNA modification, a key process in neurotoxicity. This effect persists into adulthood, suggesting m6A RNA modification is crucial in aluminum-induced neurodevelopmental toxicity.

Area of Science:

  • Neuroscience
  • Toxicology
  • Epigenetics

Background:

  • Aluminum (Al) neurotoxicity mechanisms are not fully understood.
  • Developmental exposure to aluminum may impact neuronal health.
  • m6A RNA modification is an important epigenetic regulator.

Purpose of the Study:

  • To investigate the association between developmental aluminum exposure and m6A RNA modification in mouse hippocampal neurons.
  • To determine if aluminum-induced neurotoxicity persists into adulthood.
  • To elucidate the role of m6A RNA modification in aluminum-induced neurodevelopmental toxicity.

Main Methods:

  • Pregnant mice received aluminum-lactate from gestational day 6 to postnatal day 21.
  • Offspring were assessed at postnatal day 21 and postnatal day 60.
  • Hippocampal neuron injury, m6A RNA modification levels, and methylase expression were analyzed.

Main Results:

  • Developmental aluminum exposure led to significant hippocampal neuronal injury.
  • A reduction in m6A RNA modification and methylase expression was observed.
  • Aluminum-induced neurotoxicity and reduced m6A RNA modification persisted into adulthood.
  • Continuous aluminum exposure from embryonic to adult stages exacerbated nerve damage and m6A decline.

Conclusions:

  • Aluminum-induced developmental neurotoxicity is linked to impaired m6A RNA modification.
  • m6A RNA modification plays a critical role in the neurotoxic effects of developmental aluminum exposure.
  • The findings suggest that m6A RNA modification is a key mechanism underlying aluminum-induced neurotoxicity.
Keywords:
AluminumDevelopmental toxicityM6A RNA methylationNeurotoxicity

More Related Videos

Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice10:55

Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice

Published on: March 31, 2015

10.3K
Characterizing RNA Modifications in Single Neurons Using Mass Spectrometry08:45

Characterizing RNA Modifications in Single Neurons Using Mass Spectrometry

Published on: April 21, 2022

2.4K

Related Concept Videos

Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
27.3K
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
2.6K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.7K
Role of Hippocampus in Memory01:19

Role of Hippocampus in Memory

The hippocampus, a critical brain structure, plays an essential role in memory processing, particularly in the formation and retrieval of memory. This small, seahorse-shaped region is located within the medial temporal lobe, with one hippocampus in each brain hemisphere. Experimental studies involving lesions in the hippocampi of rats have demonstrated significant impairments in tasks such as object recognition and maze navigation, indicating the hippocampus involvement in both recognition and...
2.0K
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
29
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
42