Currently, there is no universally recommended biochemical test that confirms the diagnosis in day-to-day clinical practice. An important limitation in scientific endeavour is the difficulty of clinical assessment of dementia in individuals with Down syndrome compared with the general population. Tests used to confirm dementia in the general population are not reliable or valid in populations sellckchem with congenital intellectual disability. Cognitive assessment batteries and diagnostic criteria in populations with congenital intellectual disability are required to detect dementia in the early stages and to improve studies of risk factors [4] Alzheimer’s disease starts to affect most adults with Down syndrome at about the age of 50 years (for reviews see [5,6]).

In the early-onset group, the dementia can start as early as in one’s 40s [7]. Collectively, the early-onset general population group accounts for about 1% of all cases of Alzheimer’s disease. Common neuropathology in Alzheimer’s disease The three at-risk groups for Alzheimer disease also share common endpoint neuropathologic changes in the medial temporal lobe structures and cortical areas of the brain. The mechanisms leading to these changes, however, appear to differ significantly between the groups. In other words, the cumulative brain lesions currently considered characteristic of Alzheimer’s disease should be considered as endpoints, rather than as defining aetiology of the disease [8].

The endpoint lesions consist of neuritic plaques, extra-cellular deposits of fibrillar ??-amyloid surrounded by degenerating neuronal processes and terminals, intraneural neurofibrillary tangles primarily composed of abnormally phosphorylated tau protein, vascular ??-amyloidosis associated with fibrillar amyloid deposition within the vascular wall, inflammation, and oxidative damage. It is important to highlight that two processes, excess ??-amyloid deposition and tau hyperphosphylation, contribute to these endpoint changes. These processes are toxic, presumably because they interfere with cell-to-cell communication via energy failure and with other possible mechanisms leading to neurotransmitter failure, synaptic and neuronal loss, deterioration of neuronal networks, and brain atrophy [9].

In populations of people with Down syndrome who develop dementia and in those with early-onset Alzheimer’s dementia, the characteristic brain lesions are hypothesised to develop because of various mechanisms leading to the overproduction of toxic changes and AV-951 deposits, whereas Tipifarnib myeloid in the older groups with Alzheimer’s disease there is predominance for failure of clearance mechanisms. Among the group of overproduction Alzheimer’s diseases there are multiple contributory pathways to amyloid deposition and tau hyperphosphorylation, and similarly there are, in turn, many mechanisms for the failure to clear group.