Protein aggregation, misfolding and consequential human neurodegenerative diseases

Proteins are major components of the biological functions in a cell. Biology demands that a protein must fold into its stable three-dimensional structure to become functional. In an unfavorable cellular environment, protein may get misfolded resulting in its aggregation. These conformational disorde...

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Bibliographic Details
Published in:International journal of neuroscience 2017-11, Vol.127 (11), p.1047-1057
Main Authors: Sami, Neha, Rahman, Safikur, Kumar, Vijay, Zaidi, Sobia, Islam, Asimul, Ali, Sher, Ahmad, Faizan, Hassan, Md. Imtaiyaz
Format: Article
Language:English
Subjects:
aggregation
amyloids
amyotrophic lateral sclerosis
Animals
Genetic Therapy - methods
Humans
Immunotherapy - methods
Molecular Chaperones
Neurodegenerative Diseases - drug therapy
Neurodegenerative Diseases - etiology
Neurodegenerative Diseases - therapy
pathomechanisms
Protein Aggregation, Pathological - complications
Protein misfolding
Proteostasis Deficiencies - complications
stem cell
Stem Cell Transplantation - methods
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Summary:Proteins are major components of the biological functions in a cell. Biology demands that a protein must fold into its stable three-dimensional structure to become functional. In an unfavorable cellular environment, protein may get misfolded resulting in its aggregation. These conformational disorders are directly related to the tissue damage resulting in cellular dysfunction giving rise to different diseases. This way, several neurodegenerative diseases such as Alzheimer, Parkinson Huntington diseases and amyotrophic lateral sclerosis are caused. Misfolding of the protein is prevented by innate molecular chaperones of different classes. It is envisaged that work on this line is likely to translate the knowledge into the development of possible strategies for early diagnosis and efficient management of such related human diseases. The present review deals with the human neurodegenerative diseases caused due to the protein misfolding highlighting pathomechanisms and therapeutic intervention.
ISSN:0020-7454
1563-5279
1543-5245
DOI:10.1080/00207454.2017.1286339