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Shared therapeutic options to treat Alzheimer’s Dementia

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Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive decline and dementia. It is characterized by typical pathological hallmarks like extracellular senile plaques and intracellular neurofibrillary tangles, responsible for progressive degeneration. Recent advances shed light on ...

Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive decline and dementia. It is characterized by typical pathological hallmarks like extracellular senile plaques and intracellular neurofibrillary tangles, responsible for progressive degeneration. Recent advances shed light on pathological events responsible for the progressive impairment of neuronal network activity and cell degeneration. Altered metabolic cascades on membrane proteins associated to progressive formation and accumulation of reactive species called oligomers , namely Abeta and most recently tau oligomers, appear to play the leading part of these processes. In this view most of recent literature, both from research and clinics, dedicated efforts. As a metter of fact, the future therapeutic approaches to AD will derive from these recent advances. However, besides the pathogenic process responsible for neurodegeneration, brain neuronal networks are strictly dependent on classical neurotransmitters release and activity. Neurotransmitters control cognitive functions like attention, learning and memory, as well as mechanisms of neural plasticity. Changes in neurotransmitters release is often cause of clinical manifestations observed during cognitive decline (apathy, agitation, insomnia, hallucinations, etc) as well. Although the classic view of AD refers to the cholinergic and more recently to the glutamatergic hypotheses, recent advances showed how AD largely involves almost all transmitters. This is particularly true also considering the multifaceted clinical presentation of AD. Thus, to maintain an efficient neurotransmission still remains the main pharmacological-based treatment of patients suffering from AD. However, unresolved controversies still persist about the pharmacological treatment of AD symptoms. Focus on both laboratory and clinical data useful to suggest the best therapeutic options that can be shared among specialists, to face cognitive decline symptoms during its evolution would be of great interest.


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