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Neurofilament inclusion disease (NFID) is characterized by cortical and subcortical neuronal loss and neuronal cytoplasmic inclusions composed of neuronal intermediate filament proteins.1–6 Almost all cases have presented with a syndrome typical of a frontotemporal lobar degeneration (FTLD).1–6 More recently, the clinical heterogeneity of NFID has been emphasized, with some cases presenting with parkinsonism or motor neuron disease,1 including cases resembling ALS or primary lateral sclerosis (PLS). Several cases have also had clinical and pathologic features that overlap with multiple-system atrophy (MSA).1–6
Whereas the neuronal filamentous inclusions in NFID are immunoreactive with neurofilament (NF) antibodies and negative for tau and α-synuclein,1–6 α-internexin may be the most sensitive marker for these particular inclusions.1–3 Given this observation, we investigated the frequency of NFID using α-internexin immunohistochemistry in 92 cases that had been diagnosed neuropathologically as FTLD, ALS, PLS, or MSA but in which routine screening with immunohistochemistry for NF had not been previously done.
Methods.
A consecutive series of 95 cases of diverse neurodegenerative diseases, including 3 cases of NFID, from the neuropathology files of Mayo Clinic …
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