“In the past, scientists thought that plaques and tangles, unnatural accumulations of two naturally occurring proteins in the brain, caused Alzheimer’s disease. But a research team, which included members from the Johns Hopkins University and the University of Minnesota Medical School, hypothesised that there was a specific substance in the brain that causes memory decline that is present even before nerve cells begin to die.
To test that, the team used mice whose genetic make-up was manipulated to develop memory loss much in the way people develop subtle memory problems before the earliest stages of Alzheimer’s disease. Using mice that showed early signs of memory loss and had no plaques or nerve cell loss in the brain, they discovered a form of the protein that is distinct from plaques. They extracted this protein and injected it into healthy rats. The rats suffered cognitive impairment, confirming that this protein has a detrimental effect on memory.
Once the memory-robbing protein complex is better understood, drugs could be developed to stop Alzheimer’s disease in its tracks, the researchers said. Worldwide estimates of the number of people with Alzheimer’s disease range from 15m to 20m.”
According to Wikipedia:
“Alzheimer’s disease (AD), a neurodegenerative disease, is the most common cause of dementia and characterized clinically by progressive intellectual deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes. The most striking early symptom is memory loss (amnesia), usually manifest as minor forgetfulness that becomes steadily denser with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), coordinated movement (apraxia), recognition (agnosia) and those functions (such as decision-making and planning) closely related to the frontal lobe of the brain, reflecting extension of the underlying pathological process. This consists principally of neuronal (cell) loss (or atrophy), together with deposition of amyloid plaques and neurofibrillary tangles. Genetic factors are known to be important, and polymorphisms (variations) in three different autosomal dominant genes – Presenilin 1, Presenilin 2, and Amyloid Precursor Protein – have been identified that account for a small number of cases of familial, early-onset AD. For late onset AD (LOAD), only one susceptibility gene has so far been identified – the epsilon 4 allele of the APOE gene. Age of onset itself has a heritability of around 50%.”
At present there is no cure for Alzheimer’s disease although there are treatments available which temporarily reduce degradation of the neurotransmitters and alleviate the symptoms of the disease.