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Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans

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Published on: December 18, 2016

[Neuropathology].

Yuko Saito¹, Shigeo Murayama

¹Department of Pathology and Laboratory Medicine, National Center Hospital of Neurology and Psychiatry.

Rinsho Shinkeigaku = Clinical Neurology

|January 27, 2012

Summary

Lewy body pathology in Parkinson disease (PD) and related disorders may originate in the peripheral nervous system or olfactory bulb. This alpha-synuclein aggregation then spreads through neural networks, forming Lewy body disease (LBD) phenotypes.

Area of Science:

Neuropathology
Neuroscience
Clinical Neurology

Context:

Parkinson disease (PD) and Lewy body spectrum disorders (LBD) share alpha-synuclein pathology.
Current understanding of Lewy body (LB) pathology spread is based on Braak's ascending hypothesis.
Advanced immunohistochemistry with anti-phosphorylated alpha-synuclein (p-syn) enables detailed pathological analysis.

Purpose:

To investigate alternative pathways of Lewy body (LB) pathology extension in Lewy body disease (LBD).
To examine the role of the peripheral autonomic nervous system and olfactory bulb in alpha-synuclein aggregation.
To propose a novel olfactory-amygdala extension pathway for LB pathology.

Summary:

This brain bank study combined clinical and neuropathological data to analyze Lewy body (LB) pathology.

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Researchers identified an olfactory-amygdala pathway for LB pathology spread, independent of Braak's ascending hypothesis.

Abnormal alpha-synuclein seeding in the peripheral nervous system or olfactory bulb may initiate LBD.

Impact:

Challenges existing models of Lewy body pathology progression.
Suggests potential peripheral or olfactory origins for Parkinson disease and related dementias.
Highlights the importance of alpha-synuclein in the peripheral and central nervous systems for LBD pathogenesis.