Down's dyndrome and Alzheimer's disease: dendritic spine counts in the hippocampus

Abstract

Samples of the hippocampus of four patients with Down's syndrome [two men aged 35 and 36 years with no evidence of Alzheimer's disease (AD) and two patients aged 47 and 55 years with associated AD] were obtained at post mortem and processed according to the rapid Golgi method. A significant reduction in the number of dendritic spines (DS) was found in the apical (middle, distal and oblique segments) and basilar (thick and thin segments) dendritic arbors of CA1 and CA2-3 pyramidal neurons in patients with Down's syndrome and no AD when compared to age-matched controls. An additional decrease of DS in every segment occurred in Down's patients with associated AD when compared to age-matched controls and Down's patients with no AD. In Down's syndrome (either associated or not to AD) thin basilar dendrites were the most severely involved; in AD patients CA1 pyramids were more severely affected than pyramidal neurons of the CA2-3 subfield.

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

“…The marked loss of dendritic spines in Alzheimer's disease and Down syndrome is well documented (Mehraein et al, 1975;Coleman and Flood, 1987;DeRuiter and Uylings, 1987;El Hachimi and Foncin, 1990;Ferrer and Gullotta, 1990;Baloyannis et al, 1992). Aging in rats, which is accompanied by impairments in learning, is also characterized by a substantial decrease in the frequency of axospinous synapses (Geinisman et al, 1992a).…”

Paracetamol Overdose Induces Physiological and Pathological Aberrations in Rat Brain

“…Also, mental disorders such as schizophrenia is associated with decreased density of dendritic spines in neocortical pyramidal neurons (Garey et al, 1998). In addition, patients with Down syndrome have a decreased spine density in neocortex (Takashima et al, 1989) and hippocampus (Ferrer and Gullotta 1990). On the contrary, a low dose of paracetamol may protect cerebral cortical neurons from oxidative stress and limits neuronal inflammation by reducing menadione-mediated oxidative neurotoxicity (Bisaglia et al, 2002;Tripathy and Grammas 2009).…”

In vivo MRI identifies cholinergic circuitry deficits in a Down syndrome model

“…Corresponding dendritic pathology has been characterized within the hippocampal formation and neocortex of DS patients [26,73]. Similarly within in an animal model of excitotoxic damage to the NB, cholinergic afferents modulate MAP2 expression [79], and lesions of the basal forebrain complex in neonatal mice retard the dendritic development of cortical pyramidal cells [35,64].…”