A new study published in the journal Brain overturns thinking on the role of toxic peptides in the development of Alzheimer’s disease.
Sporadic Alzheimer’s disease accounts for 99% of all Alzheimer’s cases, and involves the development of toxic peptide deposits in the brain. These peptide deposits cause the neuronal networks to be destroyed, leading to disorientation, memory loss, changes in behavior and death.
Although studies of Alzheimer’s in animal models typically use mice with mutated human genes, the new study – conducted by researchers at the University of Oslo in Norway – used a new mouse model for the more common sporadic form of Alzheimer’s.
To create this new mouse model, the function was removed from two genes in the brain that are used to excrete and digest toxic Alzheimer’s peptide beta-amyloid. The researchers say this new “transgene-free” mouse model allows studies to be conducted without “artificial overexpression” of inherited Alzheimer’s disease genes.
Although it has previously been assumed that overproduction of toxic peptides causes the onset and first clinical signs of Alzheimer’s, the new study finds that the responsible mechanism is decreased removal of toxic peptides, rather than overproduction.
The team observed that insufficient removal of toxic metabolites in the mouse model was associated with early signs of Alzheimer’s in the precise brain locations where these changes appear in humans with the disease.
In other Alzheimer’s news, a study published in the journal Alzheimer’s & Dementia and conducted by researchers at the National Hospital for Neurology and Neurosurgery in London, UK, suggests that memory loss may not always be the first sign of Alzheimer’s, as is commonly believed.
Reviewing neurology test results from a large US sample of Alzheimer’s patients, the UK team found that 1 in 5 patients in their 60s cited early symptoms unrelated to memory, although only 1 in 10 patients in their 70s had early difficulties other than memory problems.
In other words, the proportion of patients who cited early problems that were not memory related shrank with age.
Lead study author Josephine Barnes told Reuters:
“Non-memory first cognitive symptoms were more common in younger Alzheimer’s disease patients. Tests which explore and investigate these non-memory cognitive problems should be used so that non-memory deficits are not overlooked.”
Another recent Alzheimer’s study using a mouse model, which Medical News Today looked at last month, reported some success in blocking the production of beta-amyloid, which could potentially stop the disease in its tracks with minimal side effects. Mice who received the new treatment exhibited a 50% or more reduction in amyloid plaque accumulation.