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Down syndrome and Alzheimer's disease: common molecular traits beyond the amyloid precursor protein. Aging Albany NY. Augmented gene dosage, including the APP gene, could partially cause this predisposition.
Recent works have revealed that alterations in chromosome location due to the extra Chromosome 21, as well as epigenetic modifications, could promote changes in gene expression other than those from Chromosome As a result, similar pathological features and cellular dysfunctions in DS and AD, including impaired autophagy, lysosomal activity, and mitochondrial dysfunction, could be controlled beyond APP overexpression.
In this review, we highlight some recent data regarding the origin of the shared features between DS and AD and explore the mechanisms concerning cognitive deficiencies in DS associated with dementia, which could shed some light into the search for new therapeutic targets for AD treatment.
Clinical signs of dementia include a progressive decline in cognition, memory, and language. Specifically, AD is characterized by a loss of short-term memory and other mental abilities, as the neurons responsible for these skills are gradually lost. With the increase in life expectancy in most middle and developed countries, these numbers are expected to rise to million people living with dementia by [ 1 ].