Herpes simplex virus type 1 in brain and risk of Alzheimer's disease

@article{Itzhaki1997HerpesSV,
  title={Herpes simplex virus type 1 in brain and risk of Alzheimer's disease},
  author={Ruth F. Itzhaki and Woan-Ru Lin and Dazhuang Shang and Gordon Wilcock and Brian S. Faragher and Gordon A. Jamieson},
  journal={The Lancet},
  year={1997},
  volume={349},
  pages={241-244}
}

Herpes Simplex Virus Type 1 in the Brain, Apolipoprotein E Genotype and Alzheimer’s Disease

TLDR
It is confirmed that the e4 allele of apolipoprotein E is a risk factor for AD and that HSV-1, either alone or in combination with apoE, does not represent an increased risk for AD.

PCR Search for the Herpes Simplex Virus Type 1 Genome in Brain Sections of Patients with Familial Alzheimer's Disease

TLDR
Results are suggestive of limited reactivation of HSV-1, coupled with β-amyloid deposition, in the brains of individuals with familial AD.

Herpesviruses in brain and Alzheimer's disease

TLDR
Three other herpesviruses are sought in brain of elderly normal subjects and Alzheimer's disease patients: human herpesvirus 6 (HHV6)—types A and B, herpes simplex virus type 2 (HSV2) and cytomegalovirus (CMV); HHV6 is present in a much higher proportion of the AD than of age‐matched normal brains, but there is extensive overlap with the presence of HSV1 in AD brains.

Herpes simplex virus type 1 and Alzheimer’s disease

Productive herpes simplex virus in brain of elderly normal subjects and Alzheimer's disease patients

TLDR
The HSV 1 results confirm the original PCR findings that show the presence of HSV1 DNA sequences in many elderly brains, and indicate also that the whole functionalHSV1 genome is present, and that the virus has replicated.

Herpes simplex virus type 1 and Alzheimer’s disease: increasing evidence for a major role of the virus

TLDR
In relation to the potential usage of antivirals to treat AD patients, acyclovir is effective in reducing HSV1-induced AD-like changes in cell cultures, and valacy Clovir, the bioactive form of ACV, might be most effective if combined with an antiviral that acts by a different mechanism, such as intravenous immunoglobulin (IVIG).

Open peer commentary Herpes simplex virus type 1 and Alzheimer's disease

TLDR
It is discovered that herpes simplex type 1 virus is a risk factor for Alzheimer’s disease when in the central nervous system of APOE- e4 allele carriers, and it is suggested that the combination of virus and genetic factor is particularly damaging in the nervous system.

Lack of association between HSV-1 DNA in the brain, Alzheimer’s disease and apolipoprotein E4

TLDR
An association between herpes simplex type 1, ApoE4 and AD has been reported, and HSV-1 DNA was detected by the polymerase chain reaction (PCR) in the brains of 28/44 controls and 34/46 AD patients.

Herpes simplex encephalitis: involvement of apolipoprotein E genotype.

TLDR
It seems that apoE ε2 is a risk factor for HSE, based on the allele frequencies obtained from specimens from the brain or spleen of patients with HSE.

Independent and Correlated Role of Apolipoprotein E ɛ4 Genotype and Herpes Simplex Virus Type 1 in Alzheimer's Disease.

TLDR
HSV-1 and APOEɛ4 increase the risk of AD and relate to abnormal autophagy, higher concentrations of HSV- 1 DNA in AD, and formation of Aβ plaques and neurofibrillary tangles.
...

References

SHOWING 1-10 OF 26 REFERENCES

Neurotropic viruses and Alzheimer disease

TLDR
It is found that the risk of developing AD is much greater in those who are HSV1-positive in brain and who possess an apoE4 allele than for those with only one of these factors, and that the degree of damage caused by the resulting acute infection with much greater damage in the case of AD patients.

Latent herpes simplex virus type 1 in normal and Alzheimer's disease brains

TLDR
It is postulated that factors such as number or expression of viral genes and host susceptibility might be related to incidence of AD.

Herpes simplex virus type 1 DNA is present in specific regions of brain from aged people with and without senile dementia of the Alzheimer type

TLDR
The highly sensitive polymerase chain reaction has detected the viral thymidine kinase gene in post‐mortem brain from 14/21 cases of senile dementia of the Alzheimer type and 9/15 elderly normals, indicating the presence of Herpes simplex virus type 1 DNA is a region‐dependent feature of the aged brain.

Herpes simplex virus: a role in the aetiology of Alzheimer's disease?

TLDR
Investigation of an Herpes simplex virus aetiology for Alzheimer's disease using two approaches to determine if known cases of herpes encephalitis produced a similar destruction of somatostatin-containing neurons in the temporal lobe to that seen in dementia.

Herpes simplex virus genomes in human nervous system tissue analyzed by polymerase chain reaction

TLDR
The study has confirmed the previous demonstration of latent HSV in trigeminal ganglia in normal humans and assessed the frequency and distribution of HSV genomes in the nervous system tissues of patients dying of nonneurological causes.

Alzheimer's disease : advances in clinical and basic research

TLDR
Partial table of contents: DIAGNOSIS and BIOMarkers A Rational Clinical Approach to Patients with Dementia, and Pharmacotherapy of Alzheimer's Disease.

Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease

TLDR
Data support the involvement of ApoE ϵ4 in the pathogenesis of late-onset familial and sporadic AD and suggest it may operate as a susceptibility gene (risk factor) for the clinical expression of AD.

Recurrent brainstem encephalitis associated with herpes simplex virus type 1 DNA in cerebrospinal fluid

TLDR
This is the first report of the use of CSF PCR for the rapid antemortem diagnosis of herpetic brainstem encephalitis.

“Limbic Predilection in Alzheimer Dementia: Is Reactivated Herpesvirus Involved?”

  • M. Ball
  • Biology, Medicine
    Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
  • 1982
SUMMARY: In the brains of patients with senile dementia of the Alzheimer type (SDA T), the quantitatively pathognomonic neuronal lesions (tangles, plaques, granulovacuolar degeneration, Hirano