Related Experiment Video
Updated: Aug 31, 2025
09:37
A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
Published on: July 14, 2016
8.4K
HSF1, Aging, and Neurodegeneration
Alice Y Liu1,2, Conceição A Minetti3, David P Remeta3
1Department of Cell Biology and Neuroscience, Rutgers The State University of New Jersey, Piscataway, NJ, USA. liu@dls.rutgers.edu.
Advances in Experimental Medicine and Biology
|August 22, 2022
Summary
Heat shock factor 1 (HSF1) regulates protein quality control, but its function declines with age, contributing to neurodegenerative diseases (ND). Age-related changes in disordered proteins may explain HSF1 dysfunction and aggregate formation in ND.
Area of Science:
- Cellular Biology
- Neuroscience
- Biochemistry
Background:
- Heat shock factor 1 (HSF1) is a key regulator of protein quality control (QC) and proteostasis, crucial for cellular defense against stress.
- Age-related decline in HSF1 function is implicated in increased vulnerability to neurodegenerative diseases (ND).
Approach:
- This work reviews the structural, functional, and energetic aspects of HSF1 in healthy cells.
- It examines the age-dependent deterioration of HSF1 function and neuron-specific susceptibility to ND.
- The role of intrinsically disordered regions in HSF1 and disease-associated proteins is analyzed.
Key Points:
- HSF1 orchestrates the induction of heat shock proteins, essential for maintaining proteome integrity.
- Intrinsically disordered regions are a key feature of HSF1 and many proteins linked to ND.
- These disordered proteins are sensitive to age-related cellular environment changes.
Conclusions:
- A hypothesis is proposed: age-dependent alterations in the intrinsically disordered proteome are central to understanding HSF1 dysfunction and protein aggregate formation in ND.
- This perspective links fundamental aging processes to the molecular pathology of neurodegeneration.
Keywords:
AgingHSF1, Heat shock factor 1HSP, heat shock protein familyHsp, Specific heat shock proteinIntrinsically disordered proteomeNeurodegenerationProtein homeostasisMore Related Videos
Related Concept Videos
01:26Aging
164
Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
164
01:19The Effect of Aging on Tissues
2.3K
Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
2.3K
03:03Amyloid Fibrils
9.8K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
9.8K
01:37Mitochondria
14.4K
Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
14.4K
01:26Alzheimer's Disease: Overview
652
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
652
01:17Pathophysiology of Heart Failure
1.8K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
1.8K