Alzheimer's disease is very much in the news.
I have long been fascinated in the research Judith Miklossy has done finding Borrelia DNA, Lyme Disease in the hippocampus of the brains of people who had died after having Alzheimer's.
Miklossy then went on to research Alzheimer's and the role infections could have, finding spirochetes in the brains , spinal fluid and blood of patients who had died having had Alzheimer's and yet not finding them in her control group.
Judith Miklossy website is here
Of course those who follow developments with Lyme Disease are aware that in fact Alan Mac Donald previously found Borrelia DNA in the brains of patients who had died after having Alzheimer's.
Sadly not enough research is being done in this field and the controversy over the IDSA Lyme Disease Guidelines will not help science move forward.
So it was heartening to hear of this study
Neuroinflammation Screening in Immunotherapy Trials against Alzheimer's Disease.
Andreasen N, Blennow K, Zetterberg H.
Memory Clinic, M51, Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, 17176 Stockholm, Sweden.
Due to side effects in the form of meningoencephalitis in the interrupted phase II AN1792 trial of active antiamyloid β(Aβ) immunization against Alzheimer's disease (AD), there has been concern that anti-Aβ immunization may cause destructive neuroinflammation. Here, we report on two patients fulfilling clinical AD criteria who were diagnosed with Lyme neuroborreliosis during screening before inclusion in anti-Aβ immunotherapy trials. The two cases illustrate the necessity of careful biochemical screening for neuroinflammatory/neuroinfectious conditions before an AD diagnosis is made and before clinical AD patients are included in trials of therapy that could impact the immune system. Should the two cases have been included and deteriorated, additional investigations might have led to the erroneous conclusion that therapy-induced meningoencephalitis had occurred.
If only our doctors were more through in considering the role of infections as the cause of illness before putting us on Immuno -suppressants.
To quote Miklossy
Pathogens, in addition to a strong lymphoplasmocytic infiltrates, can induce slowly progressive chronic inflammation with poor or absent lymphoplasmocytic infiltrates (e.g. leprosy, syphilis). Activated macrophages and/or microglia are the principal players in this slowly progressive form of infection, which results in slowly progressive parechymal involvement and tissue atrophy.
Highest priority should be given to this emerging field of research.
It may have major implications for public health, treatment, and prevention of Alzheimer disease as adequate anti-bacterial and anti-viral drugs are available.
Treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of the disease.
The impact on reducing health-care costs would be substantial.
As it was the case for paretic dementia in syphilis, one may prevent and eradicate dementia in Alzheimer disease.