Protein Misfolding Diseases

Kolstoe, Simon; Wood, Steve

doi:10.1002/9780470572702

Cited by 30 publications

(3 citation statements)

References 183 publications

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“…The initial hypothesis that will be considered in this work is that of the Tau Hypothesis. The Tau hypothesis has long been suggested as the main step in ADZ due to the observation that the deposition of amyloid plaques does not correlate well with neuron loss [27,28]. The hypothesis promotes that a mechanism for neurotoxicity surrounds the loss of the microtubule-stabilizing tau protein which leads to the degradation of the cytoskeleton.…”

Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

“…The hypothesis promotes that a mechanism for neurotoxicity surrounds the loss of the microtubule-stabilizing tau protein which leads to the degradation of the cytoskeleton. There has not been a uniform agreement on whether tau hyperphosphorylation precedes or is caused by the formation of the abnormal helical filament aggregates [27,28]. Proponents for the hypothesis also suggest other diseases known as tauopathies link the commonality of the same protein mis-folding pattern.…”

Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

“…Proponents for the hypothesis also suggest other diseases known as tauopathies link the commonality of the same protein mis-folding pattern. In contrast, a degree of research has suggested that amyloid is the primary causative agent as seen in ADZ [27,28]. The unfortunate overall outcome of ADZ is the destruction of brain tissue resulting in loss of function and the inevitable death of the sufferer.…”

Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

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The Potential Impact of Methyl Mercury Toxicity Within Alzheimer’s Disease Progression, Considering the Tau Hypothesis, Neurovascular Hypothesis as Well as The Potential Role of Dietary and Botanical Mercury Chelators and that of Pharmacologically Developed Agents for Disease Management

Cobb

2018

APBIJ

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Alzheimer's disease (ADZ) is a devastating one that not only has a profound cost on the life of the sufferer but also upon the families, caregivers and the medical economy surrounding disease management. ADZ affects a vast human population across Northern America and indeed the world and is listed as being the 6th leading cause of death in the United States (USA).It is estimated that by 2050, there will be as many as 16 million Americans living with ADZ [1,2], and the disease progression is on a steadily increasing trajectory with an estimated new diagnosis being made every 66 seconds in the United States alone. The typical survival rate post prognosis is estimated to be between 4 to 8 years[1,2].There has been an 89% increase in deaths due to ADZ between 2000 and 2014 and it is further estimated that 1 in 3 seniors will die with some form of dementia. Nationally, ADZ affects 5.5 million Americans and has been shown to have a substantial financial cost both nationally and indeed globally. According to recent research conducted in 2016, 15.9 million family caregivers provided an estimated 18.2 billion hours and $230 billion to people with dementia. With more recent research showing that in 2017, ADZ cost the United States alone $259 billion [1,2], it is estimated that by 2050 the costs associated with dementia could be as much as $1.1 trillion [1,2]. From a global perspective, the cost of ADZ and dementia is estimated to be around $605 billion.Currently, ADZ is the only disease in the 10 leading causes of deaths in the United States that cannot be cured, prevented or slowed. It is estimated that around 1 in 10 Americans within the age bracket of 65 lives with ADZ. The future projections for disease manifestation are bleak with a projection that a 14% rise will be seen in every state across America between 2017 and 2025 [1,2]. It is currently estimated that more than 5 million Americans are currently living with ADZ, and ppopulationswithin the age range of over 85 are estimated to make up one-third of sufferers. The statistical proportion of the population with ADZ in the United States is vast, with the age group of 75-84 making the most significant percentile at 44%. Populations in the age range of 85 and above make up a 38% percentile with age ranges of 65-74 making up a 15% percentile and the age rangeof under 65s making up a 4%percentile.

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Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

Section: The Tau Hypothesis Of Adz Progressionmentioning

confidence: 99%

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The Potential Impact of Methyl Mercury Toxicity Within Alzheimer’s Disease Progression, Considering the Tau Hypothesis, Neurovascular Hypothesis as Well as The Potential Role of Dietary and Botanical Mercury Chelators and that of Pharmacologically Developed Agents for Disease Management

Cobb

2018

APBIJ

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Protein Folding in Vivo

Georgescauld

Hartl

2015

Encyclopedia of Life Sciences

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Proteins are composed of linear chains of amino acids. Upon synthesis in the cell, most proteins must rapidly acquire a specific three‐dimensional structure, a process known as folding, before they can perform their various biological functions. Productive folding is often competed by aggregation, owing to the high macromolecular crowding of the cellular environment. Moreover, the process of translation increases the danger of misfolding, as incomplete nascent polypeptides are not yet able to fold into stable structures in many cases. To avoid these off‐pathway reactions, a class of proteins called molecular chaperones has evolved in all organisms. They interact with nascent or stress‐denatured polypeptides, prevent their aggregation and assist in folding and assembly processes, often in an ATP‐regulated manner. These functions are especially important in conditions of cell stress, and their failure is linked with the manifestation of numerous age‐dependent degenerative diseases. Key Concepts Molecular chaperones are proteins that mediate folding and assembly of other proteins, without being components of the final folded or assembled structures. Molecular chaperones prevent the potentially toxic aggregation of newly synthesised polypeptides during translation and when mature proteins unfold during stress conditions or ageing. Hsp70 chaperones act as a hub in the proteostasis network by assisting protein folding and conformational maintenance and by distributing client proteins to other chaperones for correct folding. The chaperonins mediate the folding of proteins with complex topologies and kinetically frustrated folding pathways.

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Misfolded Proteins

2019

Chemical Biology of Neurodegeneration

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Protein Misfolding Diseases

Cited by 30 publications

References 183 publications

The Potential Impact of Methyl Mercury Toxicity Within Alzheimer’s Disease Progression, Considering the Tau Hypothesis, Neurovascular Hypothesis as Well as The Potential Role of Dietary and Botanical Mercury Chelators and that of Pharmacologically Developed Agents for Disease Management

The Potential Impact of Methyl Mercury Toxicity Within Alzheimer’s Disease Progression, Considering the Tau Hypothesis, Neurovascular Hypothesis as Well as The Potential Role of Dietary and Botanical Mercury Chelators and that of Pharmacologically Developed Agents for Disease Management

Protein Folding in Vivo

Misfolded Proteins

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