Focus of Research of Viral Infections Involves Neurodegenerative Diseases

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

New evidence states a viral infection brings Alzheimer’s to light. A recent editorial from the Journal of Alzheimer’s Disease shifts focus from immune system suppression to a viral infection. Dr. Douglas Kell, a professor at the University of Manchester’s School of Chemistry, claims, “We are saying there is an incontrovertible evidence that Alzheimer’s disease has a dormant microbial (viral) component. We can’t keep ignoring all of the evidence” (Knapton). Viruses are commonly found in the brains of elderly people. In most cases, they have all of their bodily functions. Around two-thirds of people will contract the viral infection herpes at some point in their lifetime. Herpes has been known to damage the central nervous system in humans.

The Herpes simplex virus or HSV is a member of the herpes virus family. HSV

The word encephalitis is derived from two Greek words. Enkephalos, which means brain, and itis, which means inflammation. Encephalitis was defined by Sir John Burton Cleland, a pathologist and naturalist. When he defined it, it was named ‘Australian X disease’.

Dementia is a syndrome which is progressive in nature, characterized by impairment of memory and loss of intellectual ability.1 Decreased level of Acetylcholine in the brain, neuro-inflammatory reaction, rise in the oxidative stress and hypercholesterolemia have been reported to play an important etiological role in the memory decline.2 Alzheimer’s Disease (AD) is the most common form of dementia which is a progressive and a neurodegenerative disease characterized by the presence of senile plaques rich in insoluble aggregates of β amyloid and neurofibrillary tangles in the brain. AD has been estimated to account for 50–60% of dementia cases in persons over 65 years of age worldwide.3 Alzheimer’s Disease International

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most widespread age-related neurodegenerative diseases. Both diseases impact a considerable number of people, where AD occurs in around 10 percent of the population greater than the age of 65 while PD occurs in roughly 1 percent of the population above the age of 65. AD is considered to be the most widespread cause of dementia, characterised by the progressive memory and cognitive deficits which impair ones day to day activities. The pathological hallmark of AD comprises of extracellular accumulation of senile plaques consisting of mainly amyloid-beta (Aβ) peptides, along with neurofibrillary tangles which are composed of the phosphorylated tau protein, located in the hippocampus and cortex. Conversely, PD is considered to be the most widespread movement disorder that is characterised by symptoms such as rigidity slow movements, resting tremor and other instabilities. The extreme loss of dopaminergic neurones in the substantia nigra is what defines PD, as the loss of this nerve cell can be linked to Lewy bodies containing aggregates of a soluble protein called α-synuclein.

Human herpes virus 7 (HHV7) is even more recently observed and is closely related to HHV6. Like other human herpes viruses, HHV6 and HHV7 are so common that most of humankind has been infected at some point, usually early in life. HHV7 can also cause roseola, but it is not clear what other clinical effects that this virus causes.

The herpes simplex virus was first mentioned as far back as 400 BC. Hippocrates wrote about symptoms of lesions. He used the word “heparin” which means to creep or to crawl. Between 14AD and 37AD Emperor Tiberius banned kissing from public festivals and ceremonies because he understood that the disease was passed from person to person. In 1893 Emile Vidal proved that the herpes simplex virus is transmitted from person to person. The virus was first isolated in 1925 by Frederic Parker and Robert N. Nye by growing the virus in vive using rabbit’s testis cells. The Herpes simplex virus is commonly known as just herpes.

Under normal condition tau binds to microtubules, stabilizing neuronal structure and integrity. Hyperphosphorylation of tau is assumed to be the cause of the formation of paired helical filaments - neurofibrillary tangles (NFT). The principle components of the senile plaques are neurofibrillary tangles in the cell bodies, neuropil threads, and neurites as well as extracellular A-beta amyloid. These lesions are surrounded by microglial and astrocytes. The brain regions affected by Alzheimer’s disease also contain neuritic or senile plaques in which extracellular deposits of amyloid are surrounded by dystrophic axons as well as the process of astrocytes and microglia. The principle constituent of amyloid is a 4kDa peptide called A-beta amyloid. A-beta amyloid is cleaved from a larger precursor protein called amyloid precursor protein. Similar abnormalities occur in transgenic mice with mutant APP and in individuals with Alzheimer’s

Alzheimer’s disease is an irreversible, neurodegenerative disease that affects the brain causing progressive memory loss and destroys thinking skills. Alzheimer’s is the most common type of dementia, which is a general term used to describe disorders that affects brain functions. Alzheimer’s disease is caused by formations of plaques and tangles in the brain. A dangerous protein called beta-amyloid tends to build up over time in the brain. As this protein molecule accumulates, they start to form plaques, which can damage and destroy brain cells. While plaques affect the spaces between the brain cells, an abnormal protein known as “tau” starts affecting inside the brain cell itself. “Tau tangles can interfere with the transportation of nutrients in and out of the cells, causing brain cells to degenerate and die” (Kosik & Bowman, 2015, p. 5). Some common symptoms for Alzheimer’s include memory loss, constantly misplacing things, unable to remember the names of family members, unable to communicate properly, and losing the ability to complete simple daily tasks. Alzheimer’s disease is a fatal disease, but patients don’t die from the disease itself. Advanced Alzheimer’s increases vulnerability and increases the chance of developing infections that soon lead to death.

There is a great deal of impetus for understanding the mechanisms that lead to clinical AD and discovering modifiable risk factors. Clinical symptoms of dementia relate to the affected areas of the brain. In AD the symptoms are caused by a progressive loss of cholinergic function due to neuronal cell death in the hippocampus and cerebral cortex, brain regions involved in thought processing and memory. At the microscopic level, the neuropathological hallmarks of AD consists of two kinds of protein aggregates, amyloid plaques and hyper-phosphorylated tangles of tau-protein (Figure 1). Amyloid precursor protein (APP) is a transmembrane protein without known function that is constitutively cleaved

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Herpes is an extremely common sexually transmitted disease in the United States. In fact, about one in four adults are infected with the virus. Some people that are affected are not completely ignoring the fact that they have the disease, but are simply unaware that they are suffering from the virus. Although the virus stays with you for life, it usually doesn’t lead to any serious life-threatening issues.

The first one is called herpes simplex virus I, HSV I and the second is herpes simplex virus II, HSV II. Both of these viruses cause herpes (blisters/sores) to appear in the oral or genital area. “HSV originated approximately 1.6 million years ago according to studies done at the University of California San Diego” (Health.UCSD.edu, 2014). The genetics of humans and primate herpes viruses were looked at because of their similarities. The studies show that the herpes virus began in ancient chimpanzees. Scientists believe that modern humans are the adaptation of these primates such as the chimpanzees and apes. After investigation of the herpes simplex virus in the chimpanzees, studies show that HSV I has been around far longer than HSV II has.

According to Dr. Richard Hunt (2016), Herpes viruses are a leading cause of human viral disease, second only to influenza and cold viruses. They are capable of causing overt disease or remaining silent for many years only to be reactivated, for example as shingles. The name herpes comes from the Latin herpes which, in turn, comes from the Greek word herein which means to creep. This reflects the creeping or spreading nature of the skin lesions caused by many herpes virus types. There are at least 25 viruses in the family Herpes viridae (currently divided into three sub-families). Eight or more herpes virus types are known to infect man frequently. Once a patient has become