Related Experiment Video
Updated: May 8, 2026
09:33
Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
SUMO and Alzheimer's disease.
Linda Lee1, Mikako Sakurai, Shinsuke Matsuzaki
1Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, 630W 168th St., New York, NY, 10032, USA.
Neuromolecular Medicine
|August 28, 2013
Summary
Small ubiquitin-like modifier (SUMO)ylation is a key regulatory process in Alzheimer's disease (AD) pathogenesis, impacting amyloid-beta and tau pathology. Understanding SUMOylation offers new therapeutic avenues for AD.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder causing dementia, characterized by amyloid-beta (Aβ) and tau protein aggregates.
- Current treatments for AD do not modify disease progression, highlighting the need for deeper understanding of AD pathogenesis.
- Small ubiquitin-like modifier (SUMO)ylation, a post-translational modification, plays critical roles in neuronal function and is implicated in AD.
Purpose of the Study:
- To review the current literature on the role of SUMOylation in Alzheimer's disease.
- To explore SUMOylated proteins and pathways potentially dysregulated in AD pathogenesis.
- To investigate how SUMOylation impacts Aβ and tau pathology and related cellular functions.
Main Methods:
- Literature review of studies on SUMOylation and AD.
- Analysis of identified SUMO substrates relevant to AD pathology.
- Discussion of SUMOylation's potential impact on Aβ processing, tau aggregation, and neuronal signaling.
Main Results:
- SUMOylation is altered in AD pathology, potentially influencing Aβ levels and tau aggregation.
- Multiple SUMO substrates are involved in synaptic physiology, mitochondrial dynamics, and inflammatory signaling, all relevant to AD.
- SUMOylation may represent a significant factor in AD pathogenesis, analogous to phosphorylation.
Conclusions:
- SUMOylation is an emerging and critical factor in Alzheimer's disease pathogenesis.
- Dysregulation of SUMOylated proteins and pathways contributes to AD.
- Further research into SUMOylation in AD may reveal novel therapeutic targets.
Related Concept Videos
01:26Alzheimer's Disease: Overview
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 and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
01:22Alzheimer's Disease: Treatment
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
01:22Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
03:03Amyloid Fibrils
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, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...