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      Neurons and Their Dendrites in Frontotemporal Dementia

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          Regional and areal patterns of cell vulnerability (manifested as cell death and neuron loss) and cell sensitivity (as revealed by the presence of intracytoplasmic inclusions) are described in patients with frontotemporal dementia (FTD) and FTD+ motor neuron disease (MND). This is followed by studies geared to learning about possible mechanisms involved in selective neuron loss and studies focused on recognizing the identity of vulnerable populations of local-circuit neurons and the impact of FTD on individual cells as well as on postsynaptic and presynaptic terminals in the frontal cortex. Neuron loss is not associated with increased vulnerability to nuclear DNA fragmentation, and nor is it accompanied by modifications in the expression of the proteins Bcl-2 and Bax, and transcription factors c-Fos and c-Jun, thus suggesting that these proteins are probably not involved in cell death in these disorders. In the frontal and temporal cortices, glutamatergic pyramidal cells and calbindin-D28k-immunoreactive GABAergic local-circuit neurons are lost in the upper cortical layers. Parvalbumin-immunoreactive cells are preserved. In addition, reduction of putative postsynaptic sites (as inferred from the decreased numbers of dendritic branches in both pyramidal and nonpyramidal neurons, and of dendritic spines in pyramidal cells) in remaining neurons of the upper layers, as well as reduction of presynaptic terminals (as suggested by the decreased expression of synaptic vesicle-associated proteins, synaptophysin, synaptotagmin, rab 3a and synapsin 1, and presynaptic plasma membrane proteins SNAP-25 and syntaxin 1) in the upper layers of the frontal cortex, but not of the posterior parietal cortex, demonstrate the combined devastating effects of FTD on cortico-cortical connections.

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          Neurotransmission: harnessing fusion machinery at the synapse.

          Neurotransmission requires the docking of synaptic vesicles to the presynaptic plasma membrane, and their signal-dependent fusion. These processes use a general 'machinery' operating at several intracellular vesicular transport steps and, in addition, use a set of unique components that characterizes this specific form of regulated secretion. This review summarizes recent progress that has significantly increased our understanding of how intracellular transport vesicles dock and fuse with their target membrane, both in the synapse and elsewhere.
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            Hippocampal and neocortical ubiquitin-immunoreactive inclusions in amyotrophic lateral sclerosis with dementia.

            Amyotrophic lateral sclerosis (ALS) patients with dementia were found to have ubiquitin-immunoreactive (IR) inclusions in the dentate granule cells of the hippocampus. These inclusions were also present in some patients with minor cognitive changes but otherwise typical ALS. Ubiquitin-IR inclusions were also found in neurons of superficial layers of the frontal and temporal cortex and in the entorhinal cortex in patients with ALS and dementia. These ubiquitin-IR inclusions were non-argyrophilic, and were not labelled by antibodies which identify Alzheimer's neurofibrillary tangles and Pick bodies, nor were they typical of cortical Lewy bodies. Our findings indicate that ubiquitin-IR inclusions in small neurons of the hippocampus, entorhinal area and neocortex are a characteristic feature of degeneration of non-motor cortex in ALS, and are particularly associated with cognitive impairment and dementia of frontal lobe type.
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              Non-invasive ion probes--tools for measuring transmembrane ion flux.

              Ionophores, used in non-invasive vibrating electrodes, can directly monitor steady-state ion flux from single cells, even when the source is non-electrogenic.

                Author and article information

                Dement Geriatr Cogn Disord
                Dementia and Geriatric Cognitive Disorders
                S. Karger AG
                July 1999
                23 July 1999
                : 10
                : Suppl 1
                : 55-60
                Unidad de Neuropatología, Servicio de Anatomía Patológica, Hospital Príncipes de España; Departamento de Biología Celular y Anatomía Patológica, Universidad de Barcelona, Campus de Bellvitge, Hospitalet de Llobregat, Spain
                51214 Dement Geriatr Cogn Disord 1999;10(suppl 1):55–60
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 15, Pages: 6


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