Personalized medicine strategies for managing patients with Parkinsonism and cognitive deficits

Metabolism: clinical and experimental (Impact Factor: 3.89). 09/2012; 62(1):S27–S29. DOI: 10.1016/j.metabol.2012.08.025


Patients exhibiting the classic manifestations of parkinsonism – tremors, rigidity, postural instability, slowed movements and, sometimes, sleep disturbances and depression – may also display severe cognitive disturbances. All of these particular motoric and behavioral symptoms may arise from Parkinson's disease [PD] per se, but they can also characterize Lewy Body dementia [LBD] or concurrent Parkinson's and Alzheimer's diseases [PD & AD]. Abnormalities of both movement and cognition are also observed in numerous other neurologic diseases, for example Huntington's Disease and the frontotemporal dementia. Distinguishing among these diseases in an individual patient is important in “personalizing” his or her mode of treatment, since an agent that is often highly effective in one of the diagnoses (e.g., l-dopa or muscarinic antagonists in PD) might be ineffective or even damaging in one of the others. That such personalization, based on genetic, biochemical, and imaging-based biomarkers, is feasible is suggested by the numerous genetic abnormalities already discovered in patients with parkinsonism, Alzheimer's disease and Huntington's disease (HD) and by the variety of regional and temporal patterns that these diseases can produce, as shown using imaging techniques.

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