**3.1 Traditional ongoing therapies**

Current pharmacological therapies (**Table 2**) for neurodegenerative diseases focus to ameliorate the life conditions of patients and are generally only palliative. Since in many cases, the aberrant deposition of the protein strongly contributes to the toxicity associated with the diseases, some treatments are currently thought to target such specific proteins (i.e., Syn and Aβ) in order to restore their correct physiological levels *in vivo.* Given the complexity in the onset and progression of these diseases, treatments should be customized and tailored to the individual needs of the patients.

In the case of AD, a therapy based on the use of cholinesterase inhibitors (ChEIs) and the N-methyl-d-aspartate (NMDA) antagonist is currently available and Food and Drug Administration (FDA)-approved. In particular, three ChEIs are used: donepezil, rivastigmine, and galantamine [81]. The aim is to increase the levels of acetylcholine, a neurotransmitter responsible for memory and cognitive function, by reducing its enzymatic breakdown. Another class is represented by NMDA receptor antagonists, such as memantine, a noncompetitive antagonist, capable to block the effects of the excitatory neurotransmitter glutamate [82]. There are


**45**

**Figure 5.**

*Polyphenols as Potential Therapeutic Drugs in Neurodegeneration*

which can reduce the metabolism of endogenous dopamine.

a series of molecules under study referred to as "disease-modifying" drugs. They should interfere with key steps in AD development, including the deposition of Aβ plaques and neurofibrillary tangle formation, inflammation, oxidative damage, iron deregulation, and cholesterol metabolism. Many drugs are proposed for their ability to alleviate behavioral symptoms of AD. A few examples include antidepressants, such as escitalopram and mirtazapine, anticonvulsants, that is, carbamazepine and levetiracetam, mood stabilizers, and stimulants, such as methylphenidate [83]. The treatments for PD are still based on dopaminergic drugs, such as levodopa, the precursor of dopamine [84]. Long-term use of levodopa determines the development of motor problems. In association with levodopa, a decarboxylase inhibitor is administered to prevent some side effects. PD therapy involves the use of dopamine agonists, such as ropinirole or rotigotine, monoamino oxidase B inhibitors, such as rasagiline and selegiline, and catechol-O-methyltransferase (COMT) inhibitors,

Novel experimental approaches are under investigation and the most promising have as a target the protein involved in the diseases. The stages of intervention could be at the level of the protein synthesis or clearance and at the level of protein aggregation or propagation of the toxic species or their precursors (**Figure 5**).

1.*Control of the protein concentration in vivo*. To reduce the production of Aβ, Tau, and Syn, the RNA interference approach is to date quite attractive [85–87]. It is based on the idea to inhibit specific protein expression by activating a sequence-specific RNA degradation process. This technology results useful to study gene function, investigate the mechanism of the disease, and validate drug targets. Of course, the suppression of the target protein might have

*New generation therapies in AD and PD. Potential levels of intervention to counteract the abnormal accumulation of the amyloidogenic proteins and restore their physiological concentration, which results from a* 

*balance between the rates of synthesis, clearance, aggregation, and propagation.*

*DOI: http://dx.doi.org/10.5772/intechopen.89575*

**3.2 New generation therapies**

#### **Table 2.** *Current available drugs for the treatment of AD and PD.*

*Polyphenols as Potential Therapeutic Drugs in Neurodegeneration DOI: http://dx.doi.org/10.5772/intechopen.89575*

a series of molecules under study referred to as "disease-modifying" drugs. They should interfere with key steps in AD development, including the deposition of Aβ plaques and neurofibrillary tangle formation, inflammation, oxidative damage, iron deregulation, and cholesterol metabolism. Many drugs are proposed for their ability to alleviate behavioral symptoms of AD. A few examples include antidepressants, such as escitalopram and mirtazapine, anticonvulsants, that is, carbamazepine and levetiracetam, mood stabilizers, and stimulants, such as methylphenidate [83]. The treatments for PD are still based on dopaminergic drugs, such as levodopa, the precursor of dopamine [84]. Long-term use of levodopa determines the development of motor problems. In association with levodopa, a decarboxylase inhibitor is administered to prevent some side effects. PD therapy involves the use of dopamine agonists, such as ropinirole or rotigotine, monoamino oxidase B inhibitors, such as rasagiline and selegiline, and catechol-O-methyltransferase (COMT) inhibitors, which can reduce the metabolism of endogenous dopamine.
