List, What I conclude from these studies is that you have to have the
gene and elevated herpes simplex virus I(elevated amounts) to develop
Alzheimer's Disease. It certainly looks like an important factor in
the development of the disease. Linda Forrest's Mom
<1>
Authors
Lin WR. Casas I. Wilcock GK. Itzhaki RF.
Title
Neurotropic viruses and Alzheimer's disease: a search for varicella
zoster
virus DNA by the polymerase chain reaction.
Source
Journal of Neurology, Neurosurgery & Psychiatry. 62(6):586-9, 1997
Jun.
Abstract
BACKGROUND: In studies on the possible role of viruses in the
aetiopathogenesis of Alzheimer's disease, herpes simplex virus type 1
(HSV1) DNA was detected by the polymerase chain reaction (PCR) in a
high
proportion of normal elderly people and of patients with Alzheimer's
disease. The combination of HSV1 and a host factor, the type 4 allele
of
the gene for apolipoprotein E, is a strong risk factor for the
disease.
METHODS: Brain specimens were examined for another herpes virus,
varicella
zoster (VZV), which, like HSV1, is neurotropic, has a predilection for
residing latently in the peripheral nervous system, and can
reactivate.
RESULTS: Using primers for sequences in the VZV origin of replication
gene
or thymidine kinase gene, VZV DNA was not found in any of 24 samples
(18
HSV1 positive), from 17 patients with Alzheimer's disease, nor in 20
samples (12 HSV1 positive from 12 aged normal people. Hybridisation of
the
PCR products with a radiolabelled oligonucleotide probe capable of
detecting less than 10 copies of the target sequence, confirmed the
absence of VZV DNA. CONCLUSION: The presence of one neurotropic
virus--HSV1--and the absence of another--VZV--in aged human brains is
consistent with a role for HSV1 in the aetiology of Alzheimer's
disease.
<2>
Itzhaki RF. Lin WR. Shang D. Wilcock GK. Faragher B. Jamieson GA.
Title
Herpes simplex virus type 1 in brain and risk of Alzheimer's disease
[see
comments].
Source
Lancet. 349(9047):241-4, 1997 Jan 25.
Abstract
BACKGROUND: The apolipoprotein E epsilon 4 (APOE-epsilon 4) allele is
a
risk factor for Alzheimer's disease (AD), but it is neither essential
nor
sufficient for development of the disease. Other factors-genetic or
environmental-must therefore have a role. By means of a PCR we have
detected herpes simplex virus type 1 (HSV1) in latent form in brains
of
elderly people with and without AD. We have postulated that limited
reactivation of the virus causes more damage in AD patients than in
elderly people without AD because of a difference in the hosts. We now
report the APOE genotypes of AD patients and non-AD sufferers with and
without HSV1 in brain. METHODS: DNA was extracted from 84 samples of
brain
from 46 AD patients (39 temporal lobe, 39 frontal lobe, three
hippocampus)
and from 75 samples of brain from 44 non-AD elderly people (33
temporal
lobe, 36 frontal lobe, six hippocampus). PCR amplification was used to
detect HSV1 thymidine kinase gene and the host APOE gene. FINDINGS: By
multiple logistic regression, the APOE-epsilon 4 allele frequency was
significantly higher in the patients positive for HSV1 in brain than
in
the HSV1-negative AD group, the HSV1-positive non-AD group, or the
HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%,
respectively).
The odds ratio for APOE-epsilon 4 in the HSV1-positive AD group
compared
with HSV1-negative non-AD group was 16.8 (95% CI 3.61-77.8) and in the
HSV1-negative AD group, 1.67 (0.21-13.4). We also compared APOE
genotypes
of 40 people who had recurrent cold sores and 33 non-sufferers; the
APOE-epsilon 4 allele frequencies were 36% and 9%, respectively (p <
0.0001). INTERPRETATION: These findings suggest that the combination
of
HSV1 in brain and carriage of an APOE-epsilon 4 allele is a strong
risk
factor for AD, whereas either of these features alone does not
increase
the risk of AD. The findings in people with cold sores support our
hypothesis that APOE-epsilon 4 and HSV1 together are damaging in the
nervous system.
eof
