Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Parkinson Disease ll: Pathophysiology

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

Alzheimer Disease ll: Pathophysiology

Alzheimer 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...

Parkinson's Disease: Overview

Parkinson's Disease: Overview

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 to...

Increased Intracranial Pressure ll: Pathophysiology

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

Encephalitis ll: Pathophysiology

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

Alzheimer Disease l: Introduction

Alzheimer 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...

You might also read

Related Articles

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

Sort by

Same author

A three-groups non-local model for combining heterogeneous data sources to identify genes associated with Parkinson's disease.

Biometrics·2026

Same author

Developmental transcriptomic analysis of cultured primary mouse cortical neurons reveals sex-specific expression of neuropeptides.

bioRxiv : the preprint server for biology·2026

Same author

Predictive Cellular Signatures from Live Human Motor Neurons Distinguish TDP-43 ALS and Enable ALS Subtype Stratification.

bioRxiv : the preprint server for biology·2026

Same author

Mechanisms controlling the deposition and dynamics of histone variant H2BE.

bioRxiv : the preprint server for biology·2026

Same author

Survey of the human proteostasis network: the ubiquitin-proteasome system.

bioRxiv : the preprint server for biology·2026

Same author

Neurogenin-2 Reprograms Human Microglial Lineage Cells into Neurons In Vitro and in Chimeric Brains.

bioRxiv : the preprint server for biology·2026

Search research articles

Related Experiment Video

Updated: May 7, 2026

Mouse Models of Periventricular Leukomalacia

Mouse Models of Periventricular Leukomalacia

Published on: May 18, 2010

PML in the Brain: From Development to Degeneration.

Erica Korb¹, Steven Finkbeiner

¹Gladstone Institutes of Neurological Disease , San Francisco, CA , USA ; Neuroscience Graduate Program, University of California , San Francisco, CA , USA.

Frontiers in Oncology

|September 25, 2013

Summary

Promyelocytic leukemia (PML) protein, previously unknown in the brain, is now found in neurons and impacts nervous system functions like development and plasticity. Further research into PML

Keywords:

Arc PML SCN circadian rhythms neocortex development neural progenitor cells neurodegeneration synaptic plasticity

More Related Videos

Human Neural Organoids for Studying Brain Cancer and Neurodegenerative Diseases

Human Neural Organoids for Studying Brain Cancer and Neurodegenerative Diseases

Published on: June 28, 2019

Isolation and Characterization of the Immune Cells from Micro-dissected Mouse Choroid Plexuses

Isolation and Characterization of the Immune Cells from Micro-dissected Mouse Choroid Plexuses

Published on: February 3, 2022

Related Experiment Videos

Last Updated: May 7, 2026

Mouse Models of Periventricular Leukomalacia

Mouse Models of Periventricular Leukomalacia

Published on: May 18, 2010

Human Neural Organoids for Studying Brain Cancer and Neurodegenerative Diseases

Human Neural Organoids for Studying Brain Cancer and Neurodegenerative Diseases

Published on: June 28, 2019

Isolation and Characterization of the Immune Cells from Micro-dissected Mouse Choroid Plexuses

Isolation and Characterization of the Immune Cells from Micro-dissected Mouse Choroid Plexuses

Published on: February 3, 2022

Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

The promyelocytic leukemia (PML) protein is a key component of nuclear bodies with diverse cellular functions.
PML's role in the nervous system was previously uncharacterized.
Recent findings indicate PML expression and function within the brain.

Purpose of the Study:

To summarize current knowledge on PML expression and function in the brain.
To highlight discrepancies and identify key areas for future research on PML in the nervous system.

Main Methods:

Literature review and synthesis of existing research on PML in the brain.
Analysis of studies investigating PML's role in neuronal function and neurodegenerative disorders.

Main Results:

PML is expressed in neurons and plays a role in brain development.
PML influences circadian rhythms and neural plasticity.
PML is implicated in the response to proteins associated with neurodegenerative diseases.

Conclusions:

PML has significant, previously unrecognized functions in the nervous system.
Despite ongoing research, the full scope of PML's role in the brain remains to be elucidated.
Future studies are crucial for understanding PML's contribution to brain health and disease.