Alzheimer’s disease (AD) is a multifactorial disease with a still barely
understood etiology. Herpes simplex virus 1 (HSV-1) has long been
suspected to play a role in the pathogenesis of AD because of its
neurotropism, high rate of infection in the general population, and
life-long persistence in neuronal cells, particularly in the same brain
regions that are usually altered in AD. The goal of this study was to
evaluate HSV-1-specific humoral immune responses in patients with a
diagnosis of either AD or amnestic mild cognitive impairment (aMCI), and
to verify the possible relation between HSV-1-specific antibody (Ab)
titers and cortical damage; results were compared to those obtained in a
group of healthy controls (HC). HSV-1 serum IgG titers were measured in
225 subjects (83 AD, 68 aMCI, and 74 HC). HSV-specific Ab avidity and
cortical gray matter volumes analyzed by magnetic resonance imaging
(MRI) were evaluated as well in a subgroup of these individuals (44 AD,
23 aMCI, and 26 HC). Results showed that, whereas HSV-1 seroprevalence
and IgG avidity were comparable in the three groups, increased Ab titers
(p < 0.001) were detected in AD and aMCI compared to HC.
Positive significant correlations were detected in AD patients alone
between HSV-1 IgG titers and cortical volumes in orbitofrontal (region
of interest, ROI1 RSp0.56; p = 0.0001) and bilateral temporal cortices (ROI2 RSp0.57; p < 0.0001; ROI3 RSp0.48; p
= 0.001); no correlations could be detected between IgG avidity and MRI
parameters. Results herein suggest that a strong HSV-1-specific humoral
response could be protective toward AD-associated cortical damage.
understood etiology. Herpes simplex virus 1 (HSV-1) has long been
suspected to play a role in the pathogenesis of AD because of its
neurotropism, high rate of infection in the general population, and
life-long persistence in neuronal cells, particularly in the same brain
regions that are usually altered in AD. The goal of this study was to
evaluate HSV-1-specific humoral immune responses in patients with a
diagnosis of either AD or amnestic mild cognitive impairment (aMCI), and
to verify the possible relation between HSV-1-specific antibody (Ab)
titers and cortical damage; results were compared to those obtained in a
group of healthy controls (HC). HSV-1 serum IgG titers were measured in
225 subjects (83 AD, 68 aMCI, and 74 HC). HSV-specific Ab avidity and
cortical gray matter volumes analyzed by magnetic resonance imaging
(MRI) were evaluated as well in a subgroup of these individuals (44 AD,
23 aMCI, and 26 HC). Results showed that, whereas HSV-1 seroprevalence
and IgG avidity were comparable in the three groups, increased Ab titers
(p < 0.001) were detected in AD and aMCI compared to HC.
Positive significant correlations were detected in AD patients alone
between HSV-1 IgG titers and cortical volumes in orbitofrontal (region
of interest, ROI1 RSp0.56; p = 0.0001) and bilateral temporal cortices (ROI2 RSp0.57; p < 0.0001; ROI3 RSp0.48; p
= 0.001); no correlations could be detected between IgG avidity and MRI
parameters. Results herein suggest that a strong HSV-1-specific humoral
response could be protective toward AD-associated cortical damage.
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