Early immunotherapy could halt Alzheimer’s progression
Progression of Alzheimer’s disease may be halted by early use of immunotherapy designed to target beta-amyloid plaques, researchers have found.
They administered anti-beta-amyloid antibodies to the hippocampus of
transgenic mice with the disease displaying both beta-amyloid plaques
and neurofibrillary tangles.
The researchers found that within three days extracellular amyloid plaques
were reduced. They also found evidence that intracellular deposits were
reduced, a phenomenon which, they believe, has not been reported before.
Importantly, two days later, the neurofibrillary tangles caused by tau
protein were also cleared and 30 days after this, when the effect of
the antibodies had diminished, the amyloid plaques were found to re-emerge,
but the neurofibrillary tangles were not.
The researchers say their findings suggest that the pathologies of amyloid
plaques and neurofibrillary tangles are linked. However, they found a
limited time period during which amyloid therapy was effective at removing
the tangles depending on the phosphorylation state of tau. Once the tangles
have become hyperphosphorylated they are resistant to the treatment.
The researchers conclude that beta-amyloid immunotherapy may be useful
for clearing both the hallmark lesions of the disease, providing that
the intervention is made early enough (Neuron 2004;43:321). |
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