Multiple sclerosis and Alzheimer's disease

Assunta Dal Bianco1, Monika Bradl, Josa Frischer

  • 1Center for Brain Research, Medical University of Vienna, Austria.

Annals of Neurology
|October 11, 2007
PubMed
Abstract

Insights

Microglia activation in multiple sclerosis (MS) cortex does not significantly influence Alzheimer's disease (AD) lesion development. Similar microglia activation patterns were observed in both MS and AD, suggesting distinct pathological drivers.

Area of Science:

  • Neuroimmunology
  • Neuropathology

Background:

  • Chronic inflammation and microglia activation are implicated in Alzheimer's disease (AD) lesion formation and Multiple Sclerosis (MS) pathology.
  • The MS cortex experiences significant inflammation, microglia activation, and demyelination, raising questions about its impact on AD lesion development.

Purpose of the Study:

  • To investigate the extent to which chronic inflammation in the MS cortex influences the development of AD lesions.
  • To compare microglia activation patterns in MS and AD cortices and their association with specific pathologies.

Main Methods:

  • Analysis of autopsy brain tissue from 45 MS cases, 9 AD cases, and 15 controls.
  • Assessment of lymphocyte and plasma cell infiltration, microglia activation, beta-amyloid plaques, neurofibrillary tangles (AT8+), and myelin pathology.

Main Results:

  • Profound and similar microglia activation patterns were observed in both MS and AD cortices.
  • Microglia activation in MS cortex correlated with meningeal lymphocyte and plasma cell infiltrates, unlike in AD and controls.
  • No significant difference in beta-amyloid plaque or neurofibrillary tangle density was found between demyelinated and non-demyelinated areas in MS cases.

Conclusions:

  • Microglia activation within the MS cortex appears to have minimal to no direct impact on the development of cortical AD pathology.
  • The findings suggest that MS-related cortical inflammation does not drive AD lesion formation.

Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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 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...
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...
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...
Alzheimer's Disease: Treatment01:22

Alzheimer'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...