The Acoustic Cortex in Alzheimer's Disease

Baloyannis, Stavros J.; Manolidis, Spiros; Manolidis, L

doi:10.3109/00016489209137072

Cited by 30 publications

(17 citation statements)

References 23 publications

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“…In our previous morphological studies on Alzheimer's disease [1,8] we described the histological and ultrastructural alterations of the cytoarchitecture in the human acoustic cortex and medial geniculate bodies, as well as alterations of the organelles in the soma and neuronal synapses [9,10]. This study is mostly concentrated on the synaptic and dendritic spine pathology of the acoustic cortex in early cases of Alzheimer's disease.…”

Section: Introductionmentioning

confidence: 96%

“…It involves a substantial number of cellular and biochemical mechanisms, characterized clinically by phenomena of cognitive decline, including a gradual impairment of communication [1].…”

Section: Introductionmentioning

confidence: 99%

“…From the neuropathological point of view Alzheimer's disease involves a number of cellular and biochemical mechanisms, characterized by selective neuronal loss [2], synaptic alterations [1,3,4], neurofibrillary degeneration and extracellular deposits of Ab peptide, in the form of neuritic plaques, which is derived from the post-translational proteolysis of AbPP [5 Á7]. …”

Section: Introductionmentioning

confidence: 99%

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Dendritic and spinal pathology in the acoustic cortex in Alzheimer's disease: morphological and morphometric estimation by Golgi technique and electron microscopy

Baloyannis

Costa

Mauroudis

et al. 2007

Acta Oto-Laryngologica

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The morphological and morphometric estimation of the acoustic cortex revealed loss of Cajal-Retzius cells in layer I, as well as an impressive abbreviation of the dendritic fields associated with loss of dendritic spines in all layers of the cortex. Numerous distorted, dystrophic and degenerated dendritic spines were also seen, which were intermixed with a considerable number of giant spines. The dendritic and spinal alterations were closely associated with mitochondrial alterations.

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Section: Introductionmentioning

confidence: 96%

“…It involves a substantial number of cellular and biochemical mechanisms, characterized clinically by phenomena of cognitive decline, including a gradual impairment of communication [1].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dendritic and spinal pathology in the acoustic cortex in Alzheimer's disease: morphological and morphometric estimation by Golgi technique and electron microscopy

Baloyannis

Costa

Mauroudis

et al. 2007

Acta Oto-Laryngologica

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“…Alterations in spine number and shape are associated with cognitive deficits in neuropsychiatric disorders and mental retardation syndromes (Blanpied and Ehlers, 2004). Dendritic spine loss has been documented in AD and in animal models, but previous studies associated such spine loss with late stages of the disease when amyloid plaques are present (Baloyannis, et al, 1992;Davidsson and Blennow, 1998;Einstein, et al, 1994;Ferrer and Gullotta, 1990;Moolman, et al, 2004;Probst, et al, 1983;Spires, et al, 2005). However, recent studies in young TG2576 transgenic mice expressing the APP-Swedish mutation observed reduced spine density prior to plaque deposition, suggesting that soluble forms of Aβ might confer synaptotoxic changes (Jacobsen, et al, 2006;Lanz, et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Rapid, concurrent alterations in pre- and postsynaptic structure induced by naturally-secreted amyloid-β protein

Calabrese

Shaked

Tabarean

et al. 2007

Molecular and Cellular Neuroscience

120

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In Alzheimer's disease increasing evidence attributes synaptic and cognitive deficits to soluble oligomers of amyloid β protein (Aβ), even prior to the accumulation of amyloid plaques, neurofibrillary tangles, and neuronal cell death. Here we show that within 1-2 hours picomolar concentrations of cell-derived, soluble Aβ induce specific alterations in pre-and postsynaptic morphology and connectivity in cultured hippocampal neurons. Clusters of presynaptic vesicle markers decreased in size and number at glutamatergic but not GABAergic terminals. Dendritic spines also decreased in number and became dysmorphic, as spine heads collapsed and/or extended long protrusions. Simultaneous time-lapse imaging of axon-dendrite pairs revealed that shrinking spines sometimes became disconnected from their presynaptic varicosity. Concomitantly, miniature synaptic potentials decreased in amplitude and frequency. Spine changes were prevented by blockers of nAChRs and NMDARs. Washout of Aβ within the first day reversed these spine changes. Further, spine changes reversed spontaneously by two days, because neurons acutely developed resistance to continuous Aβ exposure. Thus, rapid Aβ-induced synapse destabilization may underlie transient behavioral impairments in animal models, and early cognitive deficits in Alzheimer's patients.

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“…In our previous morphological studies on dementias [9][10][11], we studied the alterations of the human acoustic cortex in order to figure out the pathological background of the communication deficits, which are noticed in a large proportion of demented patients, even in the initial stages of their progressive mental decline. In this study, we attempted to proceed in morphological and morphometric estimation of the human acoustic cortex (area 41 of Brodmann) in cases of vascular dementia, focusing our observations mostly on the dendritic and spinal pathology of the neurons.…”

Section: Introductionmentioning

confidence: 99%