The corpus callosum in Pick's disease, Alzheimer's disease, and amyotrophic lateral sclerosis: Gliosis implies possible clinical consequence

Abstract

Lesions of the corpus callosum have the potential to interfere with a neurologically impaired individual's ability to function in day-to-day activities, since the corpus callosum is important for a number of higher-order activities that involve information transfer between the left and right hemispheres. Even in normal individuals, callosal lesions may lead to apraxia, agraphia, and even an alien hand syndrome whereby the person is unable to control the actions of a hand. It is easy to envisage that callosal damage could compound cognitive symptoms in individuals with dementia. However, despite the common presence of apraxia in dementia, physicians and other healthcare providers rarely focus on callosalfunction in dementia patients. The current manuscript compares pathological data from a variety of patients with dementia with age-matched control subjects showing callosal gliosis in neurodegenerative diseases including Alzheimer's disease (AD), frontotemporal dementia (FTD), and amyotrophic lateral sclerosis. We conclude that callosal gliosis is not uncommon, particularly in patients with AD and FTD. Given the severity of this pathology in some cases, we cannot exclude the possibility that it is clinically relevant. Clinical implications are discussed, and it is recommended that further studies be done to determine whether there is a relevant clinical correlate.

The HSPB8‐BAG3 chaperone complex is upregulated in astrocytes in the human brain affected by protein aggregation diseases

“…We next addressed the question whether HSPB8 and BAG3 expression may be upregulated in brain under neuropathological conditions characterized by the accumulation of misfolded aggregate‐prone proteins, including AD, PD, HD and SCA3 (Table S2). Under all these four pathological conditions, neurodegeneration is usually also accompanied by astrogliosis and microglia activation in the degenerating areas [2,42–45]. As mentioned earlier, for each disease we selected the major brain area known to exhibit early and serious neurodegeneration and compared it with the same area from age‐matched controls, as well as with another disease, where the analysed area is known to be spared from neurodegeneration (e.g.…”

“…© 2011 The Authors Neuropathology and Applied Neurobiology © 2011 British Neuropathological Society, 38,[39][40][41][42][43][44][45][46][47][48][49][50][51][52][53] …”

Evaluating the cerebral correlates of survival in amyotrophic lateral sclerosis

“…The involvement of the corpus callosum is also a frequent finding in diffusion tensor imaging (DTI) studies and is proposed to be characteristic of Wallerian‐type degeneration; however, systematic neuropathological evaluations of the corpus callosum are lacking to support that view. Few autopsy reports have provided initial support for gliosis, but not a demyelinating pathology in the corpus callosum . Phosphorylated TDP‐43 inclusions, which are considered a hallmark pathological feature of ALS, are also reportedly absent in the corpus callosum .…”

Quantitative diffusion tensor imaging in amyotrophic lateral sclerosis: Revisited

“…In general, reduction of FA has been associated with neuronal loss with astrogliosis and myelin breakdown [Beaulieu et al, 1996]. In ALS, postmortem examinations have shown neuronal loss or atrophy and ubiquitin-positive intraneuronal inclusions extending beyond the motor system in patients with ALS with and without cognitive impairment [Mackenzie and Feldman, 2003;Murray et al, 2006;Tsuchiya et al, 2002]. Also, functional imaging studies have demonstrated hypometabolism in frontal and temporal cortices [Abrahams et al, 1996;Kew et al, 1993], which further provides support for ALS as being a multisystem disease.…”