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Journal ArticleDOI

Mitotic activation: a convergent mechanism for a cohort of neurodegenerative diseases.

Jacob Husseman, +2 more
- 01 Nov 2000 - 
- Vol. 21, Iss: 6, pp 815-828
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TLDR
It is demonstrated that neurons containing characteristic lesions in a subset of diseases, including Down Syndrome, Frontotemporal Dementia linked to chromosome 17, Progressive Supranuclear Palsy, and Pick's disease, display mitotic indices, implicating diverse etiologies in mitotic activation.
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This article is published in Neurobiology of Aging.The article was published on 2000-11-01. It has received 196 citations till now. The article focuses on the topics: Pick's disease & Progressive supranuclear palsy.

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Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression

TL;DR: It is shown that mice lacking Prdx1 are viable and fertile but have a shortened lifespan owing to the development beginning at about 9 months of severe haemolytic anaemia and several malignant cancers, both of which are also observed at increased frequency in heterozygotes.
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Aggregated and monomeric α-synuclein bind to the S6′ proteasomal protein and inhibit proteasomal function

TL;DR: Binding studies demonstrate that both aggregated and monomeric α-synuclein selectively bind to the proteasomal protein S6′, a subunit of the 19 S cap, which suggests that proteasomesomal inhibition by aggregated α- synuclein could be mediated by interaction with S 6′.
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Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration

TL;DR: It is shown that Pin1 expression is inversely correlated with predicted neuronal vulnerability and actual neurofibrillary degeneration in Alzheimer's disease, providing insight into the pathogenesis and treatment of Alzheimer’s disease and other tauopathies.
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Parkin Is a Component of an SCF-like Ubiquitin Ligase Complex and Protects Postmitotic Neurons from Kainate Excitotoxicity

TL;DR: Parkin deficiency potentiates the accumulation of cyclin E in cultured postmitotic neurons exposed to the glutamatergic excitotoxin kainate and promotes their apoptosis, and parkin overexpression attenuates the accumulation in toxin-treated primary neurons, including midbrain dopamine neurons, and protects them from apoptosis.
References
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Journal ArticleDOI

Neuropathological stageing of Alzheimer-related changes.

Heiko Braak, +1 more
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
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Checkpoints: controls that ensure the order of cell cycle events

TL;DR: It appears that some checkpoints are eliminated during the early embryonic development of some organisms; this fact may pose special problems for the fidelity of embryonic cell division.
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G1 events and regulation of cell proliferation.

TL;DR: This work has shown that switches in and out of G1 are the main determinants of post-embryonic cell proliferation rate and are defectively controlled in cancer cells.
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Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease.

TL;DR: It is suggested that neuronal loss in association areas such as the superior temporal sulcus contributes directly to cognitive impairment in AD.
Journal ArticleDOI

Tau is a candidate gene for chromosome 17 frontotemporal dementia.

TL;DR: Three lines of evidence indicate that the Val279Met change is an FTDP‐17 causative mutation, and normal valine is found at this position in all three tau interrepeat sequences and in other microtubule associated protein tau homologues.
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