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Updated: Jan 29, 2026

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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
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Amyloid β perturbs elevated heme flux induced with neuronal development
Chantal Vidal1, Kelly Daescu1, Keely E Fitzgerald1
1Department of Biological Sciences, University of Texas at Dallas, Richardson, TX, USA.
Alzheimer'S & Dementia (New York, N. Y.)
|February 7, 2019
Summary
Altered heme metabolism, specifically reduced heme degradation and HO-2 levels, is an early indicator in Alzheimer's disease (AD) pathogenesis. This finding highlights heme's role in AD progression.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Heme is crucial for mitochondrial respiration and ATP generation in neurons.
- Dysfunctional heme metabolism is implicated in neurodegenerative diseases.
Purpose of the Study:
- To investigate the role of altered heme metabolism in Alzheimer's disease (AD) pathogenesis.
- To identify heme-related proteins affected in AD patients and mouse models.
Main Methods:
- Examined expression of proteins involved in heme synthesis, uptake, degradation, and function.
- Analyzed protein levels during neuronal differentiation in AD models.
- Characterized the effects of amyloid-beta (Aβ) on heme metabolism.
Main Results:
- Decreased expression of ALAS1 (heme synthesis) and HO-2 (heme degradation) observed in AD patients and mice.
- Aβ selectively reduced HO-2 levels and heme degradation.
- Heme degradation and HO-2 levels are normally elevated in differentiated neurons.
Conclusions:
- Reduced heme metabolism, particularly decreased HO-2 and heme degradation, is an early event in AD.
- Heme homeostasis is critical for neuronal function and AD pathogenesis.
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