A transgenic triple scores a home run

Article Abstract:

Studies show that cognitive deficits in amyloid precursor protein (APP) transgenic mice preceded plaques and even occurred in mouse lines with low expression of APP in which plaques never developed. Crossing in transgenes for the second genetic hit mutant presenilin 1 (PS1) accelerated pathology but did not change the phenotype and although tau mutations were not discovered in Alzheimer disease, this third genetic hit was found in frontal temporal dementia (FTD).

Genetic aspects

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A(beta) star: A light onto synaptic dysfunction?

Article Abstract:

Amyloid-(beta)*56, most likely a tetramer of A(beta) trimers, is suspected of causing early memory deficits in a mouse model of Alzheimer disease. The mechanism by which A(beta)*56 induces memory loss are not clear, but it could disrupt glutamatergic neurotransmission and thereby impair synaptic plasticity, possibly by enhancing glutamate receptor internalization, according to a research study.

Risk factors, Memory, Disorders of, Memory disorders

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Seeing what Alzheimer saw

Article Abstract:

A newly developed positron emission tomography tracer has helped in imaging fibrillar amyloid-[beta] and neurofibrillary tangles, which might help in identifying the brain pathology in living individuals with Alzheimer disease. The in vivo imaging method might help in finding a proper noninvasive diagnostic biomarker for distinguishing Alzheimer disease from other dementing disorders.

Psychological aspects, Diagnosis

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