Neuronal damage in brain inflammation

Aktas, Orhan; Ullrich, Oliver; Infante-Duarte, Carmen; Nitsch, Robert; Zipp, Frauke

doi:10.1001/archneur.64.2.185

Cited by 249Neuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research StudiesTraumatic Brain Injury and Neurovascular Disturbances

Neuronal damage in brain inflammation

Aktas, Orhan, Ullrich, Oliver, Infante-Duarte, Carmen, Nitsch, Robert, Zipp, Frauke·2007·Archives of Neurology

DOI 10.1001/archneur.64.2.185

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Abstract

In contrast to traditional textbook paradigms, recent studies indicate neuronal damage in classic neuroinflammatory diseases of the brain, such as multiple sclerosis or meningitis. In these cases, immune cells invade the central nervous system compartments, accompanied by a massive breakdown of the blood-brain barrier and typical changes of the cerebrospinal fluid. On the other hand, inflammation within the central nervous system is a common phenomenon even in classic noninflammatory brain diseases that are characterized by degeneration or trauma of neuronal structures, such as Alzheimer disease, Parkinson disease, or stroke. In these cases, inflammation is a frequent occurrence but displays different, more subtle, patterns compared with, for example, multiple sclerosis. Concepts for directly protecting neurons and axons in neuroinflammatory diseases may improve the outcome of the patients. In parallel, epidemiological and animal experimental evidences, as well as first clinical trials indicate the benefit of immunomodulatory therapies for classic noninflammatory brain diseases. We review the evidence for inflammatory neuronal damage and its clinical impact in the context of these diseases.

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Pro-inflammatory cytokines and chemokines secreted into the immediate neurological environment accelerate neuronal injury and eventually neuron death.
“Pro-inflammatory cytokines and chemokines secreted into the immediate neurological environment accelerate neuronal injury and eventually neuron death (Aktas et al., 2007; Heckmann et al., 2018; Morales et al.,2014).”
From LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease (2019) · cites this paper as Aktas et al., 2007

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Authors: Aktas, O., Ullrich, O., Infante-Duarte, C., Nitsch, R., & Zipp, F.
Affiliations: Charité – Universitätsmedizin Berlin (DE)
ORCID: Nitsch, Robert
Zipp, Frauke
Venue: Archives of Neurology
Publisher: American Medical Association (AMA)
Published: 2007-02-01
Volume: 64
Issue: 2
Pages: 185
ISSN: 0003-9942 (ISSN-L)
DOI: 10.1001/archneur.64.2.185
OpenAlex: W2101296507
Cited by: 249
References: 31
Citations by year: 2026: 12 · 2025: 11 · 2024: 14 · 2023: 16 · 2022: 39 · 2021: 17 · 2020: 13 · 2019: 20 · 2018: 11 · 2017: 13 · 2016: 11 · 2015: 5 · 2014: 9 · 2013: 9 · 2012: 8
FWCI: 7.02
Type: journal article
Language: en
Open access: closed
Locations: Archives of Neurology (publishedVersion)
PubMed (publishedVersion)
MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords: neuronal injury, neuroinflammation, multiple sclerosis, meningitis, blood-brain barrier disruption, cerebrospinal fluid, Alzheimer's disease, Parkinson's disease, stroke, neuroprotection, immunomodulatory therapy, axonal degeneration
MeSH terms: Animals, Encephalitis, Humans, Models, Biological, Neurons

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