Cited by 113Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Add Alzheimer's disease to the list of autoimmune diseases

D’Andrea, Michael R.·2005·Medical Hypotheses

Abstract

A sole pathological event leading to Alzheimer's disease (AD) remains undiscovered in spite of decades of costly research. In fact, it is more probable that the causes of AD are the result of a myriad of intertwining pathologies. However, hope remains that a single awry event could lead to the many pathological events observed in AD brain tissues thereby creating the presentation of simultaneous pathologies. Age-related vascular diseases, which include an impaired blood-brain barrier (BBB), are a common denominator associated with various degrees of dementia, including AD. Recently, a key finding not only demonstrated the anomalous presence of immunoglobulin (Ig) detection in the brain parenchyma of AD tissues but, most importantly, specific neurons that showed degenerative, apoptotic features contained these vascular-derived antibodies. In addition, subsequent studies detected classical complement components, C1q and C5b-9, in these Ig-positive neurons, which also were spatially more associated with reactive microglia over the Ig-negative neurons. Thus, it is possible that the mere presence of anti-neuronal autoantibodies in the serum, whose importance had been previously dismissed, may be without pathological consequence until there is a BBB dysfunction to allow the deleterious effects of these autoantibodies access on their targets. Hence, these observations suggest autoimmunity-induced cell death in AD.

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Crossref · 10.1016/j.mehy.2004.08.024

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  • In AD, the Aβ peptide aggregated extracellularly in neuritic plaques produces an inflammatory environment and a chronic activation of microglial and astroglial cells.

    “As mentioned above, in AD the Aβ peptide that is aggregated extracellularly in the neuritic plaques produces an inflammatory environment and a chronic activation of microglial and astroglial cells (D'Andrea, 2005).”

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Authors
D’Andrea, M. R.
Corresponding author
D’Andrea, Michael R.
Venue
Medical Hypotheses
Publisher
Elsevier BV
Published
2005-01
Volume
64
Issue
3
Pages
458-463
ISSN
0306-9877 (ISSN-L)
OpenAlex
W2116938222
Cited by
113
References
59
Citations by year
2026: 3 · 2025: 4 · 2024: 6 · 2023: 2 · 2022: 7 · 2021: 7 · 2020: 12 · 2019: 5 · 2018: 5 · 2017: 6 · 2016: 14 · 2015: 3 · 2014: 3 · 2013: 7 · 2012: 2
FWCI
3.29
Type
journal article
Language
en
Open access
closed
Locations
  • Medical Hypotheses (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, autoimmunity, blood-brain barrier dysfunction, C1q, membrane attack complex, reactive microglia, neuronal apoptosis, age-related vascular disease, dementia
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Autoantibodies, Autoimmune Diseases, Blood-Brain Barrier, Complement System Proteins, Glycoproteins, Humans, Immunoglobulin G, Neurons, Autoimmunity, Complement C1q, Complement Membrane Attack Complex

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