Alzheimer's disease and herpes viruses: Current events and perspectives.

Alzheimer's disease (AD) is a real and current scientific and societal challenge. Alzheimer's disease is characterised by a neurodegenerative neuroinflammatory process, but the etiopathogenetic mechanisms are still unclear. The possible infectious aetiology and potential involvement of Herpes viruses as triggers for the formation of extracellular deposits of amyloid beta (Aß) peptide (amyloid plaques) and intraneuronal aggregates of hyperphosphorylated and misfold could be a possible explanation. In fact, the possible genetic interference of Herpes viruses with the genome of the host neuronal cell or the stimulation of the infection to a continuous immune response with a consequent chronic inflammation could constitute those mechanisms underlying the development of AD, with possible implications in the understanding and management of the disease. Herpes viruses could be significantly involved in the pathogenesis of AD and in particular, their ability to reactivate in particular conditions such as immunocompromise and immunosenescence, could explain the neurological damage characteristic of AD. Our review aims to evaluate the state of the art of knowledge and perspectives regarding the potential relationship between Herpes viruses and AD, in order to be able to identify the possible etiopathogenetic mechanisms and the possible therapeutic implications.

A two-year longitudinal study of retinal vascular impairment in patients with amnestic mild cognitive impairment.

Objective: To evaluate the relation between retinal vascular impairment and cognitive decline in patients with amnestic mild cognitive impairment (aMCI) over time. Methods: Spectral domain-optical coherence tomography (SD-OCT) and OCT angiography study was performed in aMCI patients over 2 years follow-up and compared to baseline. Results: Thirty-eight eyes from 19 aMCI patients were evaluated. Structural and vascular OCT measures were reduced at follow-up except for vessel density (VD) of the choriocapillaris, unchanged, and foveal avascular zone, which was increased; no changes in any parameter were found in 18 age-matched healthy controls. Overall, these findings were confirmed when patients were evaluated separately according to progression to dementia. Only non-converters to dementia showed significant VD reduction in the deep capillary plexuses (coeff. ß = -4.20; p < 0.001), may be for an initial massive VD depletion becoming less evident with progression of the disease. MMSE reduction was associated with a higher ganglion cell complex reduction (coeff. ß = 0.10; p = 0.04) and a higher VD reduction in the radial peripapillary capillary (RPC) plexus (coeff. ß = 0.14; p = 0.02) in the whole patient group, while it was associated with a higher VD reduction only in RPC plexus in converters (coeff. ß = 0.21; p < 0.001). Conclusion: Our data shows vascular impairment progression in the inner retina of aMCI patients and support the hypothesis that vascular changes may contribute to the onset and progression of Alzheimer's disease. Other follow-up studies, with a larger number of patients, are needed to better define VD as a potential biomarker.