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Accumulation of calbindin in cortical pyramidal cells with ageing; a putative protective mechanism which fails in Alzheimer's disease
Author(s) -
Greene J. R. T.,
Radenahmad N.,
Wilcock G. K.,
Neal J. W.,
Pearson R. C. A.
Publication year - 2001
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.0305-1846.2001.00351.x
Subject(s) - neocortex , calbindin , temporal lobe , pathogenesis , degenerative disease , neuroscience , alzheimer's disease , neuroprotection , medicine , biology , endocrinology , central nervous system disease , pathology , disease , immunohistochemistry , epilepsy
There is considerable interest in the status of calbindin immunoreactive neurones in Alzheimer's disease (AD) but previous studies have produced widely differing results. Here we describe calbindin neurones in temporal neocortex from 18 severely demented patients with neuropathologically confirmed AD and 13 age and post‐mortem delay matched, neurologically normal controls. Calbindin immunoreactive neurones were small and round in layers II–IV, and pyramidal in layers IIIc and V. There were significantly more calbindin positive neurones in controls than in AD (mean± SD, for each comparison P < 0.01): superior temporal lobe, AD = 3.32 ± 2.24, Control (C) = 24.83 ± 10.8; middle temporal lobe, AD = 3.6 ± 4.94, C = 26.09 ± 15.7; inferior temporal lobe, AD 3.69 ± 3.6, C = 25.25 ± 16.9. Furthermore, there was an age‐related increase in immunopositive neurones in the superior ( r 2 = 0.37, P = 0.046) and inferior ( r 2 = 0.75, P = 0.01) temporal gyri in controls. In AD the number of calbindin positive neurones did not change with age. This is the first report of such an age‐related increase in controls, and it suggests that this, rather than a decrease in AD, accounts for the overall difference between AD and controls. It is possible that an increase in intraneuronal calbindin protects these cells from degeneration and that failure of such a neuroprotective mechanism is a significant contributory factor in the pathogenesis of AD.