Recent literature shows a controversial new push to tie microorganisms to
Alzheimer’s disease (AD). Study after study, in which scientists have injected human
Alzheimer-diseased brain tissue into mice and other laboratory animals that later
developed the disease have left little doubt that Alzheimer’s disease (AD) arises
from an infectious process. By 2013 Mawanda and Wallace’s “Can Infections Cause
Alzheimer’s Disease” struck down some of the commonly entertained pathogens
for AD such as herpes simplex virus type 1, Chlamydia pneumoniae, and several
types of spirochetes. Instead they pointed to two prime suspects for Alzheimer’s
amyloid-beta deposition: “especially chronic infections like tuberculosis and
leprosy.” To be sure, it was German neuropathologist Oskar Fischer of the Prague
school of Neuropathology, Alzheimer’s great rival, who was the first to suggest that
infection might be causative for Alzheimer’s. Fischer’s credentials: he was the codiscoverer
of Alzheimer’s disease. His suspected germ was the Streptothrix, today
classified as Actinomycetes, a rare central nervous system pathogen which at the
time was so constantly and consistently mistaken for tuberculosis that ChoppenJones
suggested that TB be called tuberculomycosis. And Just ten years before
Oskar Fischer found Actinomycosis-like forms in Alzheimer’s cerebral plaque,
Babèş and immunologist Levaditi reported in “On the Actinomycotic Shape of the
Tuberculous Bacilli” that Fischer’s typical Actinomyces-like clusters (Drüsen) with
clubs appeared in the tissue of rabbits inoculated with tubercle bacilli beneath
the dura mater of their brains. Investigators who supported a
'via Blog this'
Alzheimer’s disease (AD). Study after study, in which scientists have injected human
Alzheimer-diseased brain tissue into mice and other laboratory animals that later
developed the disease have left little doubt that Alzheimer’s disease (AD) arises
from an infectious process. By 2013 Mawanda and Wallace’s “Can Infections Cause
Alzheimer’s Disease” struck down some of the commonly entertained pathogens
for AD such as herpes simplex virus type 1, Chlamydia pneumoniae, and several
types of spirochetes. Instead they pointed to two prime suspects for Alzheimer’s
amyloid-beta deposition: “especially chronic infections like tuberculosis and
leprosy.” To be sure, it was German neuropathologist Oskar Fischer of the Prague
school of Neuropathology, Alzheimer’s great rival, who was the first to suggest that
infection might be causative for Alzheimer’s. Fischer’s credentials: he was the codiscoverer
of Alzheimer’s disease. His suspected germ was the Streptothrix, today
classified as Actinomycetes, a rare central nervous system pathogen which at the
time was so constantly and consistently mistaken for tuberculosis that ChoppenJones
suggested that TB be called tuberculomycosis. And Just ten years before
Oskar Fischer found Actinomycosis-like forms in Alzheimer’s cerebral plaque,
Babèş and immunologist Levaditi reported in “On the Actinomycotic Shape of the
Tuberculous Bacilli” that Fischer’s typical Actinomyces-like clusters (Drüsen) with
clubs appeared in the tissue of rabbits inoculated with tubercle bacilli beneath
the dura mater of their brains. Investigators who supported a
'via Blog this'
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