Related Experiment Video

Updated: May 28, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
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

Inflammation and the pathophysiology of Alzheimer's disease

M M Greer1

  • 1Neuroscience Research Laboratories, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, Calif, USA.

Dialogues in Clinical Neuroscience
|October 29, 2011
PubMed

Insights

Chronic brain inflammation in Alzheimer's disease (AD) drives neuronal damage and cognitive decline. Microglia activation, involving macrophage colony-stimulating factor (M-CSF), exacerbates this neuroinflammation, offering therapeutic targets.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) is increasingly linked to chronic neuroinflammation.
  • Microglia, the brain's immune cells, play a central role in AD pathogenesis.
  • Neuroinflammation contributes to neuronal injury and cognitive decline in AD.

Purpose of the Study:

  • To review the evidence for neuroinflammation in Alzheimer's disease.
  • To elucidate the mechanisms of microglial activation and neurotoxicity in AD.
  • To present evidence for macrophage colony-stimulating factor (M-CSF) in microglial activation and discuss therapeutic strategies.

Main Methods:

  • Review of existing evidence on neuroinflammation in Alzheimer's disease.
  • Description of microglial mechanisms generating neurotoxic factors (cytokines, reactive oxygen species, nitric oxide).
  • Presentation of data implicating M-CSF in microglial activation.
  • Use of organotypic hippocampal explant cultures to model AD neuroinflammation.

Main Results:

  • Microglia contribute to neurotoxicity through the release of inflammatory mediators.
  • Macrophage colony-stimulating factor (M-CSF) acts as a cofactor in microglial activation in AD.
  • Organotypic hippocampal explant cultures provide a model for studying AD-related inflammation.

Conclusions:

  • Chronic neuroinflammation mediated by microglia is a key driver of Alzheimer's disease progression.
  • M-CSF is implicated as a critical factor in microglial activation within the AD brain.
  • Targeting microglial activation pathways presents a promising therapeutic avenue for Alzheimer's disease.
Keywords:
Alzheimer's diseasecytokineinflammationmicrogliaβ-amyloid

More Related Videos

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps10:19

Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps

Published on: August 14, 2016

Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

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...
Alzheimer Disease l: Introduction01:29

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...
Alzheimer's Disease: Overview01:26

Alzheimer'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...
Parkinson Disease ll: Pathophysiology01:24

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...
Dementia l: Introduction01:22

Dementia 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...
Encephalitis ll: Pathophysiology01:26

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...