Alzheimer’s disease (AD) is the most common cause of old age-related dementia. This chronic disorder, that slowly destroys neurons and causes serious cognitive disability,
is affecting an increasing number of individuals each year. The estimated number of patients suffering from AD was nearly 30 million worldwide in 2006 and is expected to reach
above 100 million in 2050. Such prognosis points AD as an emerging social problem affecting not only patients but also their caregivers.
The neuropathological hallmarks of AD include a degeneration of synapses, a progressive loss of neurons, and a deposition of beta-amyloid plaques and tau protein tangles in cortex, hippocampus and other brain regions. Both intra- and extracellular beta-amyloid oligomers as well as cellular filaments of hyperphosphorylated tau protein alter several neuronal functions including calcium signaling, intracellular trafficking and energy metabolism. In turn, these disturbances of cellular activities lead to an increased generation of beta-amyloid and phosphorylation of tau protein and thus exacerbate neurodegeneration.
Currently available therapeutics are able to slow down the progress of AD but not to cure the disease or at least to stop its development. Today’s treatment, although beneficial, does not solve the growing problem of increasing AD prevalence.
It is our ambition to obtain an efficient drug - capable of breaking up the positive feed-back loop of AD pathogenesis. Such therapy should completely stop disease development and significantly improve patients’ cognitive abilities.
Oncology
Metabolic disorders
The neuropathological hallmarks of AD include a degeneration of synapses, a progressive loss of neurons, and a deposition of beta-amyloid plaques and tau protein tangles in cortex, hippocampus and other brain regions. Both intra- and extracellular beta-amyloid oligomers as well as cellular filaments of hyperphosphorylated tau protein alter several neuronal functions including calcium signaling, intracellular trafficking and energy metabolism. In turn, these disturbances of cellular activities lead to an increased generation of beta-amyloid and phosphorylation of tau protein and thus exacerbate neurodegeneration.
Currently available therapeutics are able to slow down the progress of AD but not to cure the disease or at least to stop its development. Today’s treatment, although beneficial, does not solve the growing problem of increasing AD prevalence.
It is our ambition to obtain an efficient drug - capable of breaking up the positive feed-back loop of AD pathogenesis. Such therapy should completely stop disease development and significantly improve patients’ cognitive abilities.
OncologyMetabolic disorders
Celon Pharma Ltd
ul. Ogrodowa 2A
05-092 Lomianki, Kielpin
ul. Ogrodowa 2A
05-092 Lomianki, Kielpin
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Designed by GREGMAR