• Bugs in the brain 04 July 2018 | View comments

  • 04th July 2018 | By David Jolley

    So much to think about and so much to study from the report of the Gosport Inquiry - I was pleased to take a look into another world of investigation into possible causes or complications of Alzheimer’s disease. There had been interest in the idea that viruses might play a part in causation – observations going back to the 1950s but new research offers detailed which demonstrate viral materials in excess ‘abundance’ in the brains of people with Alzheimer’s disease – especially in those regions most closely associated with cognition and the other changes which occur in the condition. https://www.theguardian.com/society/2018/jun/21/alzheimers-link-to-herpes-virus-in-brain-say-scientists

    1970s saw measles as able to cause an acute encephalitis – but also a delayed condition subacute sclerosing panencephalitis: the concept was established that a virus could linger for years within the Central Nervous System – apparently without causing symptoms or damage to the neurones, only to assume a more destructive presence after a period of years. 

    Amongst the early investigators to suggest that herpes viruses might be implicated was Dr Ruth Itzaki – now Professor at Manchester University – working with Dr Richard Sutton at Withington Hospital. Richard Sutton was a virologist who established a small laboratory within the Psychogeriatric Unit which we ran as part of the first special service for older people with mental health problems in the North West of England. 

    Many reports have followed – often citing HerpesViride, HHV-6, HHV-7 as the viruses most likely to be implicated. 

    Recent reports suggest that microbes such as these can stimulate amyloidosis as a reaction to their presence in the CNS. This brings together the idea of an invasive virus underlying the emergence of pathological changes we recognise as characteristic of Alzheimer’s disease. 

    The study by Readhead et al reviews careful analyses of the brains of normal people, patients with pre-clinical Alzheimer’s Disease and patients with clinical Alzheimer’s Disease.

    In studies of tissue from 3 independent clinical cohorts HHV 6A and HHV-7 are more abundant in Alzheimer’s disease> Tissue from Superior temporal Gyrus (STG) (137), Anterior Prefrontal Gyrus (APFG) (213), Inferior Frontal Gyrus (IFG) (186) and Parahippocampal Gyrus (PHG) (107). 

    They looked for the presence of 515 viruses – entire viral sequences and individual genomes. The consistent finding was increased abundance of HHV 6A and HHV 7. 

    They looked for supportive evidence from other published cohorts - post-mortem data from: Religious Order Study (300), Memory and Ageing Project (298) and Mayo Temporal Cortex Study (278). 

    They did indeed find supportive evidence – the findings from these studies sum to a conclusion: multiple viruses are increased in multiple brain areas in Alzheimer’s Disease – predominantly HHV 6A and HHV 7 and Roseoloviruses. NB these excesses were not found in tissues from cases of other degenerative brain diseases such as Progressive Supra-nuclear Palsy (from the Mayo TC study).

    The question posed is: Is there chromosomal integration of HHV-6A with host DNA? – It looks possible i.e. the viral DNA changes the host DNA to a pathological formulation which will generate abnormal ‘alien’ proteins.

    Neuronal loss: The studies looked for apoptosis (the death of cells which occurs as a normal and controlled part of an organism's growth or development), necroptosis (Necroptosis is a programmed form of necrosis, or inflammatory cell death. Conventionally, necrosis is associated with unprogrammed cell death resulting from cellular damage or infiltration by pathogens, in contrast to orderly, programmed cell death via apoptosis.) and autophagy. This gave a measure of loss of neurones by these processes.

    They found a ‘strong negative relation between the neuronal fraction and the presence of HHV 6A’. i.e = where there was evidence of viral material, there was also evidence of neuronal loss.

    It is an exciting new insight into the basics neuroscience of the most common dementia. What it means in terms of potential for prevention, treatment or cure will be debated – and then explored experimentally.

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