Alzheimer\u27s disease-like dystrophic neurites characteristically associated with senile plaques are not found within other neurodegenerative disease unless amyloid β-protein deposition is present

Swollen, bulbous-shaped (dystrophic) neurites are a common pathologic feature of Alzheimer\u27s disease (AD) and represent one of the most abundant neuritic abnormalities within the brains of patients with this disease. In the present study, we sought to determine whether the dystrophic neurites which are observed in association with senile plaques are unique to AD or whether they are characteristic of a more generalized process of neuritic and/or neuronal degeneration which can be observed in other neurodegenerative diseases. To accomplish this, we examined post-mortem brain material from patients with AD, Parkinson\u27s disease (PD), Parkinson\u27s disease with associated AD, Parkinson\u27s disease with dementia yet without AD pathology, Huntington\u27s disease (HD), Pick\u27s disease and normal age-matched controls (NC). Using a battery of antibodies to amyloid β-protein (AβP), paired-helical filaments (PHF), tyrosine hydroxylase, substance P, neurotensin, and somatostatin we found that immunolabeled dystrophic neurites of the type characteristically observed in AD, were seen only in cases and in brain regions where AβP deposition was present. More specifically, brain areas known to display severe afferent and/or local degenerative changes such as the caudate and putamen in all three PD groups, the caudate in the HD cases, and the temporal cortex in the HD and Pick\u27s cases were conspicuously free of these swollen neurites unless AβP deposition was also present. While these findings did not exclude the possibility that other forms of neuritic degeneration may accompany the degeneration seen in these other diseases, they do suggest that the enlarged immunolabeled neurites so frequently observed in AD brains are unique to AD and in particular are restricted to brain regions with β-amyloid deposits. © 1993