Alzheimer’s disease causes 50-70% of all dementias and is a leading cause of mortality. The prevalence of Alzheimer’s disease is about one percent at age 65 and increases dramatically to between 20-50% in those older than 85 years. The pathological hallmarks of Alzheimer’s disease are extracellular accumulation of amloid β (Aβ) peptide in the brain (“senile plaque” SP) and by intraneuronal accumulation of hyper-phosphorylated tau protein in neurofibrillary tangles (NFT). This is accompanied by synaptic and neuronal losses. Neuropathological criteria of Alzheimer’s disease are based on density and distribution of SP and NFT in the brain. Thus, the pathological diagnosis is Alzheimer type pathology, while the diagnosis of dementia relies on clinical information. Lewy body disease are other common dementias, which present themselves clinically as Dementia with Lewy bodies or Parkinson disease dementia (PDD). There is commonly a large degree of overlapping Alzheimer’s disease and Lewy body pathology in demented individuals.
Key knowledge gaps both nationally and internationally limit our understanding of the etiology and molecular pathogenesis of dementia. These mechanisms need to be elucidated in order to identify novel therapeutic targets that can prevent disease progression. Furthermore, better biomarkers for dementia diagnosis and progression need to be identified. Biomarkers would be of particularly high value in dementa as neurodegeneration is already advanced at the time of clinical diagnosis. Furthermore, biomarkers are necessary to provide surrogate endpoints to evaluate the clinical efficacy of new neuroprotective therapies. Hence, biomarkers are pivotal to identify patients with prodromal dementia that may be ideal candidates for neuroprotective therapies.
Neuro-SysMed currently runs the following clinical studies on dementia:
Last updated 12/2/2024