Abstract
Chronic neurodegenerative diseases are complex, and their pathogenesis is uncertain. Alzheimer’s disease (AD) is a neurodegenerative brain alteration that is responsible for most dementia cases in the elderly. AD etiology is still uncertain; however, chronic neuroinflammation is a constant component of brain pathology. Infections have been associated with several neurological diseases and viruses of the Herpes family appear to be a probable cause of AD neurodegenerative alterations. Several different factors may contribute to the AD clinical progression. Exogeneous viruses or other microbes and environmental pollutants may directly induce neurodegeneration by activating brain inflammation. In this paper, we suggest that exogeneous brain insults may also activate retrotransposons and silent human endogenous retroviruses (HERVs). The initial inflammation of small brain areas induced by virus infections or other brain insults may activate HERV dis-regulation that contributes to neurodegenerative mechanisms. Chronic HERV activation in turn may cause progressive neurodegeneration that thereafter merges in cognitive impairment and dementia in genetically susceptible people. Specific treatment for exogenous end endogenous pathogens and decreasing pollutant exposure may show beneficial effect in early intervention protocol to prevent the progression of cognitive deterioration in the elderly.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative brain alteration that is responsible for most dementia cases in the elderly
HHV-6A and EBV induced human endogenous retroviruses (HERVs)-K18-encoded superantigen and host T-cell responses to such super antigen could secondarily lead to local autoimmune phenomena
Data are on record showing that the human immunodeficiency virus (HIV) Rev protein can functionally interact with many repetitive elements (RcREs) present in the human genome, depending on the
Summary
Tau intra neuronal deposition is a neurodegenerative hallmark of AD and tau pathology is found in a heterogeneous group of neurodegenerative syndromes, the tauopathies, causing cognitive and/or motor impairment. Differential expression for several retrotransposons in association with neurofibrillary tangle burden was observed in serial RNA sequencing from human AD brains [37] These results highlight evidence for global transposable elements (TE) transcriptional activation among the LINE-1 and ERV clades I. We suggest that neuro infection agents such as exogenous neurotropic virus, other human pathogens with neuro damage potential, and chemical environmental insults might cause ERV activation by inducing brain temporary immune responses and inflammation. We suggest that microbes’ infections of human CNS may directly induce inflammation and neurodegeneration, but they may activate brain HERV which in turn by acting as continuous abnormal stimulation of inflammatory responses may contribute to neurodegenerative hallmarks associated with AD
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