Overexpression of amyloid precursor protein (APP), as well as mutations in the APP and presenilin genes, causes rare forms of Alzheimer's disease (AD). These genetic changes have been proposed to cause AD by elevating levels of amyloid-beta peptides (Abeta), which are thought to be neurotoxic. Since overexpression of APP also causes defects in axonal transport, we tested whether defects in axonal transport were the result of Abeta poisoning of the axonal transport machinery. The result of the study rejected the hypothesis suggesting that APP-induced axonal defects are not caused by Abeta.
COBISS.SI-ID: 143853
On the example of certain neurological disorders, particularly extrapyramidal diseases (parkinsonism, chorea, Tourette syndrome) and dementia (Alzheimer's dementia) authors tackle the problem of free will. This used fore centuries to dwell in the domains of philosophy, theology and law. With the emergence of modern cognitive neuroscience and new diagnostic methods this problem is entering the domain of clinical neurology. From the point of volition, movements can be divided into four groups: voluntary, partially voluntary, involuntary and automatic. Main methods in the study of volition are functional neuroimaging (fMRI) and electrophysiology. Results of the studies postulate that voluntary