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Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

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Apraxia phenotypes and frontotemporal lobar degeneration.

Tobias C Langheinrich^1,2, Jennifer C Thompson^3,4, Matthew Jones^3,5

¹Cerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK. tobias.langheinrich@nca.nhs.uk.

Journal of Neurology

|October 10, 2024

Summary

This summary is machine-generated.

Apraxia in frontotemporal lobar degeneration (FTLD) varies by pathological subtype. Tau pathologies often present with dominant apraxia, while TDP-A pathology links it to communication disorders.

Keywords:

Apraxia Corticobasal syndrome Progranulin Progressive aphasia TDP pathology Tau pathology

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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

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Area of Science:

Neuroscience
Neurology
Pathology

Background:

Apraxia is a common symptom across frontotemporal lobar degeneration (FTLD) subtypes.
The precise cognitive and motor underpinnings of apraxia in FTLD remain incompletely understood.
This research aimed to elucidate apraxia characteristics within distinct pathological FTLD classifications.

Purpose of the Study:

To investigate the varied clinical presentations of apraxia across different pathological subtypes of frontotemporal lobar degeneration (FTLD).
To explore the relationship between specific FTLD pathologies (tau vs. TDP) and the manifestation of apraxia symptoms.
To differentiate the cognitive and motor substrates contributing to apraxia in FTLD.

Main Methods:

Retrospective analysis of 115 pathologically confirmed FTLD cases from a specialized cognitive neurology center.
Identification of patients with documented apraxia as a significant clinical feature.
Systematic recording of apraxia characteristics, demographics, cognitive/neurological findings, and imaging data.

Main Results:

Eighteen FTLD patients with apraxia were identified: 12 with FTLD-tau (including corticobasal degeneration, Pick type, progressive supranuclear palsy) and 6 with FTLD-TDP (type A).
Apraxia as a primary symptom was more common in FTLD-tau, whereas in FTLD-TDP it often co-occurred with aphasia.
Apraxia predominantly affected specific body parts (face/limb) in FTLD-tau but not FTLD-TDP; speech apraxia was linked to FTLD-tau.

Conclusions:

Apraxia exhibits diverse characteristics depending on the FTLD pathological subtype.
Apraxia in corticobasal degeneration (CBD) aligns with probable corticobasal syndrome (CBS) criteria, unlike in Pick-type pathology.
Apraxia in FTLD-TDP-A is viewed as part of a broader communication deficit, highlighting the need for prospective studies on FTLD apraxia substrates.