Different fibrillar Aβ 1–42 concentrations induce adult hippocampal neurons to reenter various phases of the cell cycle

Majd, Shohreh; Zarifkar, Asadollah; Rastegar, Karim; Takhshid, Mohammad Ali

doi:10.1016/j.brainres.2008.04.050

Cited by 51 publications

(47 citation statements)

References 24 publications

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“…Previous studies have shown that adult neurons are capable of regenerating in permissive environments [25,27]. We confirm that application of BDNF, GDNF and TGF-b3 enhances survival, neurite growth and regeneration of DA neurons.…”

Section: Neurotrophic Factors Are Capable Of Promoting the Survival Asupporting

confidence: 86%

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Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase-Expressing Dopaminergic Neurons

et al. 2011

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The loss of nigral dopaminergic (DA) neurons is the disease-defining pathological change responsible for progressive motor dysfunction in Parkinson's disease. In this study, we sought to establish a culture method for adult rat tyrosine hydroxylase (TH)-immunoreactive DA neurons. In this context, we investigated the role of fibroblast growth factor 2 (FGF2), brain-derived neurotrophic factor (BDNF), transforming growth factor-β3 (TGF-β3), glial-derived neurotrophic factor (GDNF) and dibutyryl-cyclic AMP (dbcAMP) in these cultures. Culturing in the presence of FGF2, BDNF and GDNF enhanced the survival of DA neurons by 15-fold and promoted neurite growth. In contrast, dbcAMP promoted neurite growth in all neurons but did not enhance DA cell survival. This study demonstrates that long-term cultures of DA neurons can be established from the mature rat brain and that survival and regeneration of DA neurons can be manipulated by epigenetic factors such as growth factors and intracellular cAMP pathways.

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Section: Neurotrophic Factors Are Capable Of Promoting the Survival Asupporting

confidence: 86%

“…The nature of the culture medium at the time of tissue dissociation and plating may also be critical to both short-and long-term neuronal survival. Methods for culturing adult rat neurons have been established [25][26][27] but have yet to be validated for midbrain DA neurons.…”

Section: Introductionmentioning

confidence: 99%

Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase-Expressing Dopaminergic Neurons

et al. 2011

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“…The abortive cell cycle re-entry has been reported in the brain of patients and in most AD animal models, 24,35,36 as well as in cultured neurons exposed to Aβ peptides. 23,35 Interestingly, in several pathologies in which ectopic cell cycle events have been described, Cdk5 overactivation also occurs.…”

Section: Discussionmentioning

confidence: 97%

“…23,35 Interestingly, in several pathologies in which ectopic cell cycle events have been described, Cdk5 overactivation also occurs. 6,9,10,25,37 However, little is known about the connection between both events.…”

Section: Discussionmentioning

confidence: 99%

Cdk5 acts as a mediator of neuronal cell cycle re-entry triggered by amyloid-β and prion peptides

Lopes

Oliveira²,

Agostinho³

2009

Cell Cycle

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“…Several different features from AD, such as amyloid, tau or oxidative stress, can be related to cell cycle re-entry [104,[112][113][114]. However, it is not clear whether the re-expression of cell cycle proteins occurs as a result of these AD pathological events or if, oppositely, cell cycle re-entry is a trigger for the development of AD-associated alterations.…”

Section: Alzheimer's Disease and Cell Cycle Re-entrymentioning

confidence: 96%

Cell Cycle Re-Entry in Alzheimers Disease: A Major Neuropathological Characteristic?

Lopes¹,

Oliveira²,

Agostinho

2009

CAR

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Alzheimer's disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. With over 26 million patients in 2006, AD is the most prevalent neurodegenerative disease worldwide. Different hypotheses have been suggested to explain the pathogenesis of AD, like those involving inflammation, mitochondrial dysfunction or oxidative stress. Many of these studies have addressed amyloid plaque formation, tau hyperphosphorylation and apoptotic neuronal loss, the three main histopathological hallmarks of this disease. Increasing evidences, however, suggest another feature that can also be considered a neuropathological marker for AD: ectopic cell cycle re-entry. Cell cycle events have been frequently registered in the brains of AD patients. Although the exact starting point of cell cycle re-entry remains unclear, a number of subsequent cascades, which include events such as kinase upregulation, DNA replication and cytoskeletal alterations, have already been described. There are also increasing reports suggesting that cell cycle reactivation in mature neurons occurs as part of the apoptotic process. Upon a brief overview of the different theories and models addressing cell cycle reactivation in AD, we will describe possible mechanisms that trigger cell cycle re-entry, with special attention to links between this feature and the main neuropathological markers of AD. Finally, we will also analyze possible similarities between cell cycle dysregulation in AD and in other pathologies, such as Prion-Related Encephalopathies.

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Different fibrillar Aβ 1–42 concentrations induce adult hippocampal neurons to reenter various phases of the cell cycle

Cited by 51 publications

References 24 publications

Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase-Expressing Dopaminergic Neurons

Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase-Expressing Dopaminergic Neurons

Cdk5 acts as a mediator of neuronal cell cycle re-entry triggered by amyloid-β and prion peptides

Cell Cycle Re-Entry in Alzheimers Disease: A Major Neuropathological Characteristic?

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