Increased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease

Jiang, Yu; Wang, Xiu Li; Cao, Xue Hong; Ye, Zengyou; Li, Li; Cai, Wen Qing

doi:10.1016/j.brainres.2013.04.059

Cited by 63 publications

(60 citation statements)

References 22 publications

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“…The following discussion focuses on HSF1 inducers and their role in nurturing brain tissues, whether through canonical or non-canonical pathways. But first we note that loss of HSF1 activity is associated with neurodegeneration (Kondo et al 2013;Jiang et al 2013;Verma et al 2014). Most recently, α-synuclein, a protein associated with Parkinson's disease, has been found to accelerate HSF1 protein degradation, while HSF1 activation in turn limits α-synuclein accumulation (Kim et al 2016).…”

Section: Hsf1 Inducers and Cognitive Preservationmentioning

confidence: 99%

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The central role of heat shock factor 1 in synaptic fidelity and memory consolidation

Hooper

Durham

Török

et al. 2016

Cell Stress and Chaperones

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Networks of neuronal synapses are the fundamental basis for making and retaining memory. Reduced synapse number and quality correlates with loss of memory in dementia. Heat shock factor 1 (HSF1), the major transcription factor regulating expression of heat shock genes, plays a central role in proteostasis, in establishing and sustaining synaptic fidelity and function, and in memory consolidation. Support for this thesis is based on these observations: (1) heat shock induces improvements in synapse integrity and memory consolidation; (2) synaptic depolarization activates HSF1; (3) activation of HSF1 alone (independent of the canonical heat shock response) augments formation of essential synaptic elementsneuroligands, vesicle transport, synaptic scaffolding proteins, lipid rafts, synaptic spines, and axodendritic synapses; (4) HSF1 coalesces and activates memory receptors in the postsynaptic dendritic spine; (5) huntingtin or α-synuclein accumulation lowers HSF1 while HSF1 lowers huntingtin and α-synuclein aggregation-a potential vicious cycle; and (6) HSF1 agonists (including physical activity) can improve cognitive function in dementia models. Thus, via direct gene expression of synaptic elements, production of HSPs that assure high protein fidelity, and activation of other neuroprotective signaling pathways, HSF1 agonists could provide breakthrough therapy for dementia-associated disease.

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Section: Hsf1 Inducers and Cognitive Preservationmentioning

confidence: 99%

“…Therefore, HSF1 appears to play a core role in the consolidation of memory complexes through generation of PSD and lipid rafts. This ultimately leads to coalescence and activation of memory receptors, synapse and dendrite stabilization, and long-term memory retention (Jiang et al 2013). …”

Section: Pathways Of Hsf1 Activationmentioning

confidence: 99%

The central role of heat shock factor 1 in synaptic fidelity and memory consolidation

Hooper

Durham

Török

et al. 2016

Cell Stress and Chaperones

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“…Thus, HSP60 deficiency might be a common cause of mitochondrial dysfunction, which is a significant observation since AD has been classically described as a disorder aggravated by oxidative stress and/or mitochondrial defect characterized by protein conformation abnormalities [98,99]. Expression of HSP60 is significantly decreased in the parietal cortex of AD subjects and in the cerebella of a rat model of AD, suggesting a defect in the protective role of this chaperonin in the AD brain [99,100].…”

Section: Hsp60: Biomedical and Molecular Aspectsmentioning

confidence: 95%

Chaperonotherapy for Alzheimer’s Disease: Focusing on HSP60

Cappello

Gammazza

Vilasi

et al. 2015

Heat Shock Proteins

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“…Expression of Hsp60 is significantly decreased in the parietal cortex of AD subjects and in the cerebella of a rat model of AD, suggesting a defect in the protective role of this chaperonin in the AD brain [81,83]. In support of the neuroprotective effects of Hsp60, it has been demonstrated that in a human neuroblastoma cell line, induced expression of the chaperonin prevented intracellular -amyloid-induced inhibition of complex IV and consequently reduced apoptosis [84].…”

Section: Hsp60mentioning

confidence: 98%

Alzheimer's Disease and Molecular Chaperones: Current Knowledge and the Future of Chaperonotherapy

Gammazza¹,

Bavisotto²,

Barone³

et al. 2016

CPD

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Abstract:Background: Alzheimer's disease (AD) is a dementia, a neurodegenerative condition, and a protein-misfolding disease or proteinopathy, characterized by protein deposits, extracellular plaques and intracellular neurofibrillary tangles, which contain the AD's typical pathological proteins, abnormal -amyloid and hyperphosphorylated tau, respectively, and are located predominantly in the cortex of the frontal, parietal, and temporal brain lobes.

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Increased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease

Cited by 63 publications

References 22 publications

The central role of heat shock factor 1 in synaptic fidelity and memory consolidation

The central role of heat shock factor 1 in synaptic fidelity and memory consolidation

Chaperonotherapy for Alzheimer’s Disease: Focusing on HSP60

Alzheimer's Disease and Molecular Chaperones: Current Knowledge and the Future of Chaperonotherapy

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