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Spatial transcriptomics reveals molecular dysfunction associated with cortical Lewy pathology.

Thomas M Goralski^1,2, Lindsay Meyerdirk^1,2, Libby Breton^1,2

¹Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, 49503, USA.

Nature Communications

|March 27, 2024

Summary

This summary is machine-generated.

Researchers identified specific cortical neurons vulnerable to Lewy pathology in Parkinson's disease (PD). They discovered a conserved molecular dysfunction signature (LAMDA) in affected neurons, impacting synaptic and mitochondrial functions.

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Area of Science:

Neuroscience
Molecular Biology
Genomics

Background:

Lewy pathology, primarily α-synuclein aggregates, is a hallmark of Parkinson's disease (PD) and related dementias.
While dopaminergic neuron vulnerability in PD is known, cortical neuron susceptibility to Lewy pathology and its molecular consequences remain poorly understood.

Purpose of the Study:

To identify specific cortical neuron subtypes vulnerable to α-synuclein pathology.
To characterize the molecular changes within cortical neurons bearing Lewy pathology.

Main Methods:

Spatial transcriptomics was employed to analyze whole transcriptome signatures in human and mouse cortical neurons with and without α-synuclein pathology.
Comparative analysis was performed across human PD, dementia with Lewy bodies, and a mouse model of α-synucleinopathy.

Main Results:

Specific classes of excitatory neurons were found to be vulnerable to Lewy pathology in both human patients and a mouse model.
A conserved gene expression signature, termed Lewy-associated molecular dysfunction from aggregates (LAMDA), was identified in aggregate-bearing neurons.
LAMDA signature involves downregulation of synaptic, mitochondrial, and cytoskeletal genes, and upregulation of DNA repair and immune-related genes.

Conclusions:

This study pinpoints vulnerable cortical neuron populations in Parkinson's disease.
A conserved molecular dysfunction signature (LAMDA) provides insights into the cellular mechanisms underlying Lewy pathology in the cortex.
Findings contribute to understanding cognitive decline in PD and related synucleinopathies.