Apathy is one of the most frequent behavioral disturbances in many neurodegenerative disorders and is known to have a negative impact on the disease progression, particularly in Alzheimer's disease. Therapeutic options are currently limited and non-pharmacological approaches should constitute first line treatments. Pharmacological agents likely to reduce apathy levels are lacking. The objective of the present article is to review recent pharmacological treatments for apathy in neurodegenerative disorders. The Pubmed database was searched with a particular focus on articles published as of January 2017. Current main levels of evidence have been reported so far with cholinergic, glutamatergic and dopaminergic agents to reduce levels of apathy, despite several conflicting results. Treatment duration and samples sizes may have however decreased the validity of previous results. Ongoing studies involving more participants/treatment duration or distinct neural pathways may provide new insights in the treatment of apathy in neurodegenerative disorders.
Parkinson's disease (PD) and Alzheimer's disease (AD) are common neurodegenerative disorders of the elderly and, therefore, affect a growing number of patients worldwide. Both diseases share, as a common hallmark, the accumulation of characteristic protein aggregates, known as Lewy bodies (LB) in PD, and neurofibrillary tangles in AD. LBs are primarily composed of misfolded α-synuclein (aSyn), and neurofibrillary tangles are primarily composed of tau protein. Importantly, upon pathological evaluation, most AD and PD/Lewy body dementia cases exhibit mixed pathology, with the cooccurrence of both Lewy bodies and neurofibrillary tangles, among other protein inclusions. Recent studies suggest that both aSyn and tau pathology can spread and propagate through neuronal connections. Therefore, it is important to investigate the mechanisms underlying aggregation and propagation of these proteins for the development of novel therapeutic strategies. Here, we assessed the effects of different pharmacological interventions on the aggregation andinternalization of tau and aSyn. We found that anle138b and epigallocatechin gallate decrease aSyn aggregation, that fulvic acid attenuates aggregation of the repeat domain of tau, and that dynasore reduces tau internalization.Establishing the effects of small molecules with different chemical properties on the aggregation and spreading of aSyn and tau will be important for the development of future therapeutic interventions.
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