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antiviral Treatment for AD?
The involvement of HSV1 in AD suggests that antiviral agents might prevent further deterioration of patients, and possibly, in the future, vaccination against HSV1 might prevent the development of AD. Future clinical trials should investigate the usage of antiherpetics such as acyclovir (ACV), and its biodrug valacyclovir (which is converted to ACV), in AD sufferers. ACV crosses the normal blood–brain barrier and causes few side effects, apart from in patients with renal impairment. ACV has been used for treating MS patients (based on the putative role of another herpes virus in MS) and a clinical trial showed that it crossed the blood–brain barrier, that no patients demonstrated a damaged barrier [Lycke et al. 2003] and that even a dosage of 3 g per day for 2 years caused no visible ill effects [Friedman et al. 2005].
ACV is a nucleoside analogue that stops viral replication. Its action depends on the presence of HSV1 thymidine kinase (TK). TK phosphorylates ACV to its monophosphate form, and then cell enzymes further phosphorylate it to the diphosphate and triphosphate forms. The triphosphate competes with dGTP as a DNA polymerase substrate and so it prevents chain elongation in newly forming DNA. Thus, ACV 'finds' HSV1-infected cells and stops virus replication.
Another possible agent is intravenous immunoglobulin (IVIG), which acts by a completely different mechanism from that of ACV and other anti-HSV1 antiviral agents in current use for acute HSV1 disorders such as HSE (and cold sores). IVIG products are derived from the pooled plasma of thousands of people, so they contain large amounts of neutralizing antibodies to a number of microbes, including HSV1. IVIG is able not only to neutralize any extracellular virus but also to help destroy cells acutely infected with HSV1 [Kohl and Loo, 1986]: a useful feature as the virus can be transferred from cell to cell without release of extracellular virus. In murine models of HSE, IVIG was found to protect against death and it reduced the number of trigeminal ganglia containing latent HSV1 [Erlich and Mills, 1986].
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One potential problem with the use of IVIG in AD is that it might have only limited access to the brain, but there is evidence that the blood–brain barrier is permeable in AD [Pahnke et al. 2009] and so it is likely that IVIG would enter AD patients' brains. In fact, IVIG has been tried in a few AD patients for a totally different purpose, namely, to augment their relatively low level of anti- Aß antibodies, with the aim of enhancing the clearance of Aß. A very small-scale retrospective study of patients treated with 0.4 g/kg every 2 weeks for 3.5–6 months found that IVIG was well tolerated, and that neurocognitive test scores were either stable or otherwise showed trends toward improvement in some aspects [Devi et al. 2008]. A subsequent equally small study of patients with mild AD showed that anti- Aß antibodies in serum increased proportionately to IVIG dose, and that 'mini-mental state' scores increased during treatment [Relkin et al. 2009]; interestingly, use of monoclonal anti- Aß antibodies did not lead to similar encouraging effects on cognitive function, suggesting perhaps that the IVIG had affected some factor other than Aß. Further, a recent retrospective study has shown that prior treatment with IVIG (at least once during a 3-year period) reduces the risk of developing AD in patients aged 65 years or over, compared with untreated controls (although over 30% of those treated with IVIG had cancer diagnoses, and so their lower risk of AD might have reflected their associated treatments and diagnoses [Fillit et al. 2009]). It is unknown whether in these studies there was an IVIG-induced anti- HSV1 action (especially in APOE-e4 carriers, as it is the combination of HSV1 in brain and APOE-e4 that confers risk of AD, but unfortunately no data on APOE genotypes were presented). However, an anti-HSV1 action might explain the apparent paradox that monoclonal Aß did not have the same beneficial effect as IVIG.
Currently available anti-HSV1 antiviral agents work by stopping viral DNA synthesis and therefore they prevent only the damage caused by the virus that is initiated as a consequence of viral DNA synthesis. Thus, they might be ineffective against damage occurring independently of viral DNA synthesis, for example damage resulting from viral attachment to the cell membrane or viral entry into the cell. However, we have found that the HSV1-induced formation of Aß and of AD-like tau occurs only after synthesis of the first group of viral proteins following viral entry: the so-called immediate–early (IE) proteins [Wozniak, Frost, Preston, and Itzhaki, unpublished observations]. Consistently, preliminary experiments with ACV show that its addition to HSV1-infected cell cultures does indeed decrease greatly the levels of Aß and of AD-like tau in the cells (as well as viral replication, as expected
Antiviral agents, unlike other treatments that are available or are being tested, would provide a completely new approach in that they would inhibit a major cause of the disease rather than inhibiting the consequences/symptoms (Aß, Aß oligomers or AD-like tau). In addition, by targeting a cause of AD, not only would Aß, Aß oligomers or AD-like tau be prevented but other products that might be involved in AD pathogenesis would also be inhibited.