Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

659
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...
659
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

931
Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
931
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

687
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
687
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

256
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...
256
Amyloid Fibrils03:03

Amyloid 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,...
9.8K
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

3.9K
Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
3.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Region-specific dysregulation of proline metabolic enzymes underlying mitochondrial dysfunction in the postmortem brains of patients with schizophrenia.

Journal of psychiatric research·2026
Same author

The dual role of Schlafen11 in brain tumors: Jekyll and Hyde.

Expert review of anticancer therapy·2026
Same author

Transcriptomic and pathological analysis of the hnRNP network reveals glial involvement in frontotemporal lobar degeneration pathological subtypes.

Brain communications·2026
Same author

Bacterial transfer-messenger RNA activates antiviral RNA sensing to induce inflammatory innate immune responses.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

Early oligodendrocyte dysfunction signature in Alzheimer's disease: Insights from DNA methylomics and transcriptomics.

Molecular psychiatry·2026
Same author

A protective role for APP in nuclear waste clearance via lysosomal exocytosis.

Proceedings of the National Academy of Sciences of the United States of America·2026

Related Experiment Video

Updated: Sep 3, 2025

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

11.6K

Pathological substrate of memory impairment in multiple system atrophy.

Yasuo Miki1,2, Kunikazu Tanji1, Kana Shinnai1

  • 1Department of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Neuropathology and Applied Neurobiology
|July 30, 2022
PubMed
Summary

Pathological alpha-synuclein in the hippocampus causes memory loss in multiple system atrophy (MSA). This study links alpha-synuclein oligomers in hippocampal neurons to memory impairment in MSA patients and models.

Keywords:
memory impairmentmultiple system atrophyneuronal cytoplasmic inclusionα-synucleinα-synuclein oligomer

More Related Videos

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

17.5K
Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

10.3K

Related Experiment Videos

Last Updated: Sep 3, 2025

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

11.6K
Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

17.5K
Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

10.3K

Area of Science:

  • Neuroscience
  • Pathology
  • Molecular Biology

Background:

  • Synaptic dysfunction in Parkinson's disease (PD) stems from alpha-synuclein propagation.
  • Multiple system atrophy (MSA) involves abnormal alpha-synuclein in oligodendrocytes and is linked to memory impairment.
  • Previous work associated memory deficits in MSA with hippocampal alpha-synuclein-positive neuronal cytoplasmic inclusions (NCIs).

Purpose of the Study:

  • To investigate the mechanism by which abnormal alpha-synuclein in the hippocampus leads to memory impairment in MSA.
  • To explore the role of alpha-synuclein oligomers in hippocampal synaptic dysfunction and memory deficits in MSA.

Main Methods:

  • Pathological and biochemical analyses were conducted on a mouse model of adult-onset MSA and human MSA, PD, Alzheimer's disease, and control brain tissues.
  • Behavioral and physiological assessments were performed on the MSA mouse model.
  • Quantification of NCIs, alpha-synuclein oligomers, and dendritic spine density, along with electrophysiological recordings (long-term potentiation), were utilized.

Main Results:

  • In the MSA model, alpha-synuclein expression in oligodendrocytes preceded accumulation in hippocampal neurons (NCIs) and memory impairment.
  • Increased alpha-synuclein oligomers and decreased dendritic spine density were observed in the hippocampus of MSA model mice, correlating with impaired long-term potentiation.
  • Human MSA cases with memory impairment exhibited more hippocampal NCIs and alpha-synuclein oligomers compared to those without.

Conclusions:

  • Alpha-synuclein oligomers accumulating in hippocampal excitatory neurons are implicated as a pathological cause of memory impairment in MSA.
  • These findings highlight a potential therapeutic target for memory dysfunction in MSA.