Sunday, 26 July 2015


Alzheimer's Disease
Studied with Autopsy demonstrates  that Infection by Borrelia Spirochetes
is regularly present in Autopsy Alzheimer's Disease brains. The Chronic Borrelia Brain Infection is a Cause of Alzheimer's Disease.

The Model  for  Dementia CAUSED by Chronic  brain Infections by Spirochetes is the conclusive Model of Dr. Hideyo Noguchi  who proved that Treponema Pallidum  late chronic Brain Infection is  THE CAUSE  of General Paresis 
[ Syphilis dementia]

21st century tools investigate infection by detection of microbe's DNA at the site of the Disease in human tissue.

DNA of Borrelia is Present in the following areas of the Alzheimer's Brain:
1.  All of the Alzheimer's Plaques
2.  Perfect Spirochetes (Borrelia) are seen under the fluorescent microscope
       in solid brain tissues, in Blood vessels of the Brain, and in the   Alzheimer's Plaques.
3.  All of the Granular bodies which are present in dying nerve cells in the     Alzheimer's Brain
        (Granulo-vacuolar Degeneration: {GVB Lesions]
Autopsy Brain, when placed in Laboratory Cultures produce pure Cultures of Borrelia spirochetes.

My present Research uses DNA Probes , specific for borrelia , to bind to  sites in diseased brain tissues, specifically Alzheimer's Disease Autopsy Brain tissues.

FISH methods (Fluorescence In Situ DNA Hybridization)-  in my research -  utilizes the BEST DNA PROBES available today, specifically Molecular Beacons.  The Molecular Beacons absolutely bind to Target Borrelia DNA ...
but only will bind to a DNA .. if There is a 100% match-
between TheMicrobe Borrelia DNA in diseased tissues - and the DNA structure in My  Molecular Beacon DNA Probes...
            If even a single Base (nucleotide "A"or"T" ,or"G", or "C") Mismatch exists, .. the 100% rule for Molecular Beacon Binding is Violated,.
and no signal will be released by the DNA probe.  A positive signal indicates that the 100% match rule for Molecular Beacon DNA Probe binding has been satisfied.  A Positive FISH Hybridization in Alzheimer's Brain,  is Bulletproof evidence of Borrelia infection - Visualized by the Fluorescent Microscope.
FISH Borrelia Probes Visualize ENTIRE Borrelia spirochetes - at the EXACT sites of Alzheimer's tissue injuries..

In a Series of  cases from the Harvard Brain Bank ,

         [from Alzheimer's Disease Brains]..
my Molecular Beacon DNA Probes bound to Borrelia DNA in ALL CASES STUDIED. (5/5)

The astonishing observation in my DNA probe studies on the Harvard Brain Bank Alzheimer's Disease Cases is the Discovery of not just One Borrelia,  But, Two strains of borrelia in five of five Alzheimer' s brains...
Two different   species of Borrelia spirochetes
(Burgdorferi and Miyamotoi)  were simultaneously present in the Alzheimer's Brain tissues, from Harvard.

The Discovery of Burgdorferi  in Alzheimer's Brain was FIRST published by me in the Journal of the American Medical Association in 1986.  
I demonstrated Borrelia spirochetes from 4 cases obtained from Dr. George Glenner's Brain Bank at the UCSD SanDiego.
I succeeded in a total of 6 Alzheimer's Cases in the culture in the laboratory of Living Borrelia spirochetes from DEAD (Autopsy Brain) tissue., between 1986 to 1988. 
Subsequently, in year 1993,  Cultures for borrelia from Autopsy Alzheimer's disease  was again verified by Dr. Judith Miklossy, in Switzerland.

In year 2015, my research continues, with DNA probes specific for Borrelia DNa in Alzheimer's tissue. I request your support to extend my DNA Probe studies
to connect Chronic Deep Brain Infection with Borrelia Burgdorferi and Borrelia Miyamotoi in Alzheimer's patients. I want to extend my research to study the
Spinal fluid from living Donor patients with Dementia to detect Borrelia DNA in the spinal Fluid.

Early Detection of Borrelia Brain Infection offers the opportunity for the patient to be treated in the hope that ERADICATION of Brain and Spinal Fluid Infection, can Prevent the Development of Dementia.

I thank you for your support.  All of my research has always been FREE for All , and will remain Free for All.
None of my discoveries have been or ever will be patented .  No patient / volunteer will ever be charged for my research on their Behalf.

Respectfully submitted,

Alan B. MacDonald,MD
Fellow, College of American  Pathologists

8427 Benelli Court
Naples. Florida, 34114, USA

Note: Additional Video Lectures on my Alzheimer's Research  are FREEly available on You Tube and Vimeo.

My Website:

I have posted Images /Galleries of Borrelia spirochetes
under Fluorescent Microscopy  using my FISH method
and my Borrelia Specific DNA Probes:

Taken and shared from Dr MacDonald's Fund Raiser - raising funds for further research into the links between various Borrelia species and Alzheimer's.

Please give generously and share this fundraiser among your friends (also at this link Dr MacDonald has updated details and presentations on his important work)

Link to Poster presentation of Dr MacDonald's research

Friday, 24 July 2015


Penetration of doxycycline into cerebrospinal fluid in patients treated for suspected Lyme neuroborreliosis.

  1. L Hagberg

      Twelve patients were treated orally with 100 mg of doxycycline twice a day (b.i.d.) and 10 patients were treated with 200 mg b.i.d. for suspected tick-borne neuroborreliosis (Lyme borreliosis). At 5 to 8 days after the start of therapy, the mean concentrations in serum were 4.7 micrograms/ml for the doxycycline dose of 100 mg b.i.d. and 7.5 micrograms/ml for 200 mg b.i.d., 2 to 3 h after the last drug administration. The corresponding levels for cerebrospinal fluid were 0.6 and 1.1 micrograms/ml. Since a doxycycline concentration in cerebrospinal fluid above the estimated MIC for Borrelia burgdorferi (0.6 to 0.7 microgram/ml) is wanted in patients treated for severe neuroborreliosis, the higher dose is preferable.
    2. Minocycline versus Doxycycline in the Treatment of Lyme Neuroborreliosis

    3. 'It is not commonly appreciated that ill patients treated with doxycycline (e.g., patients with legionnaires' disease) should be given a loading regimen of 200 mg iv q12h for the first 72 h, because of doxycycline's lipid solubility characteristics and long half-life. Since 5 serum half-lives are usually required to achieve steady-state serum concentrations, and early therapeutic effect, a loding regimen rather than a loading dose permits rapid saturation of the serum. If doxycycline is administered in the usual dosage of 100 mg q12h, then it takes 4–5 days to achieve steady-state kinetics and an observable therapeutic response. In Lyme neuroborreliosis, rapid saturation of the CNS compartment is key to the efficacy of short-course regimens (≤14 days). Doxy-cycline is usually given in dosages of 100 mg q12h, which means that the first week of treatment is virtually lost in achieving steady-state equilibrium, and equilibrium results require 3 weeks [710]. Dotevall and Hagberg correctly used 400 mg of doxycycline daily and decreased treatment time to ∼10.8 days.'

    4. Although the above articles were published some years ago I have posted them because they support the need for a higher dose of Doxycycline in the treatment of early Lyme Neuroborreliosis. A concept foreign to most of our doctors. Lyme Neuroborreliosis is when the bacteria affect the nervous system and the symptoms are many and varied the best resource for details about Lyme Neuroborreliosis is found in the leaflet Lyme Disease Action have on the subject. It is easy for patients and doctors to say it is suspected Lyme Disease and fail to realise the significance of nervous system symptoms indicating Lyme Neuroborreliosis.

Sunday, 5 July 2015


Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection


Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with Bburgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B.burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that Bburgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain ofBburgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of Bburgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that Bburgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.

Author Summary

Infections with the Lyme Disease agent, Borrelia burgdorferi, often fail to generate long-term protective immunity. We show here that this is because the immune system of the Borrelia-infected host generates only short-lived, structurally abnormal and non-functional germinal centers. These germinal centers fail to induce memory B cells and long-lived antibody-producing plasma cells, leaving the host susceptible to reinfection with Bb. This inability to induce long-term immunity was not due to the nature of Borrelia antigens, as even T-dependent antigens of Borrelia were unable to induce such responses. Moreover, influenza vaccine antigens, when applied during Borrelia-infection, failed to induce strong antibody responses and immune-protection from influenza challenge. This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which Bburgdorferi subverts the adaptive immune response.