Selective loss of inhibitory neurons in the cerebral cortex in motor neuron disease

Introduction:  The pattern of β-amyloid (Aβ) deposition in cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD) suggests that Aβ is eliminated along perivascular interstitial fluid drainage pathways. The age at which accumulation of Aβ in the brain becomes significant in AD coincides with the development of cerebrovascular disease (CVD) and increasing rigidity of artery walls through arteriosclerosis.
Hypothesis:  The distribution of Aβ deposits in Alzheimer brains is influenced by CVD.
Materials and methods:  Paraffin sections of frontal, parietal, temporal and occipital lobes from six cases with Alzheimer's disease were stained for reticulin and by immunocytochemistry for Aβ and GFAP.
Results:  Three distinct patterns of Aβ deposition were seen in relation to cortical blood vessels: (i) early deposition of Aβ in cortical parenchyma was related to individual cortical arterial territories; (ii) severe capillary amyloid angiopathy and an absence of Aβ plaques were associated with thromboembolic occlusion of the feeding artery; (iii) Aβ plaques were abundant in areas devoid of capillary amyloid angiopathy.
Conclusions:  The pattern of Aβ deposition corresponds to individual intracortical arterial territories, and hence periarterial ISF drainage territories. Cerebrovascular disease influences the pattern of Aβ deposition within brain parenchyma and in vessel walls in individual arterial territories. Failure of periarterial drainage of Aβ from the brain may be related to cerebrovascular disease and is possibly due to altered arterial pulsations.