Regulating dopamine levels could reduce symptoms in the early stages of Alzheimer's disease. Countering the 'memory thief' with therapies already available for Parkinson's is the scenario that opens up thanks to a study conducted by Campus Bio-Medico University (Ucbm) and the Santa Lucia Irccs Foundation of Rome. On experimental models, scientists confirmed that “dopaminergic stimulation is effective in reducing hyperexcitability of the hippocampus, a condition underlying the onset of epilepsy and which may contribute to progressive cognitive damage in Alzheimer's disease”.
In Italy over 600 thousand people live with this pathology still without a cure, the leading cause of dementia. Although to date the diagnosis is exclusively linked to the symptoms reported to the neurologist by the patient and measured by the neuropsychologist – Ucbm recalls – research is proposing more and more solutions to recognize Alzheimer's early. A promising area concerns the study of the areas of the brain responsible for the production of dopamine, a neurotransmitter whose deficit is usually linked to Parkinson's disease, for which numerous therapies already exist. In this context, the team of Marcello D'Amelio, head of the Molecular Neuroscience Laboratory of the Irccs Santa Lucia and full professor of Human Physiology of the Campus Bio-Medico University, has focused for some years on the ventral tegmental area (Vta ), a brain area linked to the production of dopamine and involved in numerous functions as a 'crossroads' of different circuits of the brain, which connect different parts. In the new study, D'Amelio's group confirmed that dopamine levels in the hippocampus, the brain area where memory is located, play a role in the long pre-clinical phase of Alzheimer's, characterized by cortical hyperexcitability and small epileptic episodes often asymptomatic and detectable with electroencephalographic investigations.
“Acting even before the patient shows obvious symptoms of the disease – explains the specialist – is very complex. To achieve this it is necessary to identify with reasonable certainty the patient who will actually develop the disease and intervene as soon as possible to preserve the neurons. In fact, not all patients with the typical lesions of Alzheimer's develop the disease and our previous clinical study on Vta has made it possible to identify very early the patients who will develop Alzheimer's disease by isolating them from those who, despite presenting amyloid lesions, are less risk. With this study we add a further piece to the knowledge of the preclinical phases of Alzheimer's. By intervening on the dopaminergic mechanisms of the brain with drugs well known for their effectiveness in Parkinson's disease, we have succeeded, in experimental models and not yet on humans – specifies D'Amelio – to preserve neuronal activity in areas affected by the disease, reducing hippocampal hyperexcitability which can lead to epileptic activities typical of the initial phases of Alzheimer's disease, and contribute to the worsening of cognitive decline”.
The mechanism triggered by the lack of dopamine, in turn linked to an early degeneration of the Vta – explains a note – prevents correct activation of interneurons which have the function of controlling cortical excitability. Ultimately, the new study confirms the importance that dopaminergic circuits play in Alzheimer's disease, historically linked to the deficiency of other neurotransmitters including acetylcholine. “This is a promising area of research – the experts point out – because it would allow the therapies currently available for Parkinson's disease to be transferred to Alzheimer's disease”.
“The early and accurate diagnosis of Alzheimer's disease – points out D'Amelio – is essential for selecting patients who must undertake specific therapeutic paths, including pharmacological ones, including therapies with monoclonal antibodies against beta-amyloid. It is in fact clear that the more the earlier the start of treatment, the greater the chances of slowing down or hopefully stopping the cognitive deterioration that leads the patient to complete loss of autonomy. This work – he concludes – goes in the direction of identifying specific alterations of cortical excitability as biomarkers of disease which, together with others currently available, can better characterize the stage of development of the disease and help the clinician to undertake the most suitable therapeutic path”.
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