Abstract
Alzheimer's disease (AD) is one of the principal causes of disability and morbidity. It is one of the most expensive illnesses. Despite this, there are no significant data regarding its etiology and optimal treatment. This review concentrates on the viral hypothesis of AD. After a comprehensive PubMed literature search, we analyzed the studies associating herpes simplex virus type-1 (HSV1) infection to AD from the previous 10 years. Molecular mechanisms whereby HSV1 induces AD-related pathophysiology, including neuronal production and accumulation of amyloid-beta (amyloid-β), abnormal phosphorylation of tau proteins, impaired calcium homeostasis, and autophagy, are addressed. The virus also imitates the disease in other ways, showing increased neuroinflammation, oxidative stress, synaptic dysfunction, and neuronal apoptosis. Serological studies correlate HSV1 infection with AD and cognitive impairment. A causal link between HSV1 and AD raises the concept of a simple, efficient, and preventive treatment alternative. Anti-viral agents impede brain degeneration by preventing HSV1 spread and its replication, decreasing hyperphosphorylated tau and amyloid-β; thus providing an efficacious treatment for AD. We also mention brown algae, intravenous immunoglobulin (IVIG), and a synthetic drug, BAY57-1293, with anti-viral properties, as options for treating AD. We want to recommend future researchers to look for more affordable, non-invasive, and swifter techniques to identify HSV1 in the brain and assist in the early detection and prevention of AD.
Highlights
Background"Alzheimer's disease locks all the doors and exits
The deleterious consequences of herpes simplex virus type-1 (HSV1) infection imitate the vital aspects of Alzheimer's disease (AD) pathophysiology
Numerous studies have enlisted mechanisms used by HSV1 to prompt chief processes involved in the formation of unique signs of AD, namely, amyloid plaques and neurofibrillary tangles
Summary
"Alzheimer's disease locks all the doors and exits. There is no reprieve, no escape.". Harris et al concluded that interactions between cytokines and the brain after crossing the BBB is the likely mechanism of neuropathology and brain dysfunction [15] Another aspect highlighted by Itzhaki et al linking HSV1 to AD, is lysosomal impairment due to interactions between HSV1 infection and oxidative stress leading to the accumulation of toxic substances, further accelerating neurodegenerative changes (Figure 2) [33]. A parallel investigation validated that the accumulation of AD hallmarks in the same mice's brain displayed impaired memory in behavioral tests [29] These findings demonstrate that HSV1 infection of neuronal cells can generate multiple APP fragments with neurotoxic potentials (Figure 3) [29]. Harris et al imply that amyloid plaque results from immunologic warfare between host and HSV1 [15]
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