## 1 Introduction  
The incidence of neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease (PD), is progressively rising due to the natural increase in life expectancy [1; 2; 3; 4; 5; 6].  
AD is the most common neurodegenerative disease and the most frequent form of dementia. The neuropathological hallmarks of AD are the aggregates of amyloid-beta and tau proteins [7; 8; 9], whereas the clinical spectrum is characterized by progressive cognitive decline. Patients first suffer from loss of episodic memory, and later develop a multidomain deterioration with functional disability. Based on the aetiology, two formsof AD can be distinguished: the familial, more rare, and the sporadic, which instead represents the vast majority of cases. Familial AD forms depend on pathogenic variants in three main genes, namely the amyloid precursor protein (_APP_), presenilin 1 (_PSENI_), and presenilin 2 (_PSEN2_). Conversely, sporadic AD has a multifactorial origin, due to the interaction between genetic risk factors (e.g., variants in genes implicated in cholesterol metabolism and neuroinflammation) and other acquired factors (e.g., mid-life hypertension or diabetes) [10]. In addition, more recently, a potential pathogenic role has been recognized for microwaves. Indeed, microwave radiation can affect the human brain, interfering with the neurochemical transmission in critical areas for memory and cognition, such as the hippocampus. Moreover, it may exert detrimental neuronal effects, as preclinical models have shown, that can account for an increased risk of neurodegeneration in exposed individuals [11].  
PD, instead, is the second most common neurodegenerative disease whose core neuropathological features are the loss of dopaminergic neurons in the substantia nigra pars compacta and the brain accumulation of alpha-synuclein-positive Lewy bodies [12; 13; 14]. The clinical presentation of PD includes a triad of motor signs: bradykinesia, rigidity, and rest tremor. However, a wide spectrum of nonmotor symptoms (e.g., constipation, mood disturbances, sleep disorders, etc.) accompanies the disease course, from prodomal to advanced stages. As for AD, only a minority of PD cases are inherited, whereas the largest part depends on a complex interplay between genetic background and other risk factors (age, male sex, rural living, and exposure to certain pesticides).  
Even if effective disease-modifying treatments are not available for these disorders, several symptomatic drugs can be used with a remarkable impact on the quality of life [15; 16; 17; 18]. In particular, AD patients can benefit from medications potentiating cholinergic signaling and enhancing memory circuits. PD patients, conversely, take advantage from drugs that increase dopamine in the nigrostriatal pathway.  
Oral, enteral, and parenteral administrations are considered the gold standard for drug delivery, although with some limitations and restrictions. In fact, at later disease stages of AD and PD, dysphagia and swallowing difficulties may provide an obstacle to the assumption of the tablets [19]. Moreover, in PD, a narrowing of the therapeutic window occurs along the disease progression, with consequent long-term side effects of Levo-Dopa treatment (i.e., motor fluctuations and dyskinesia) [20]. In this perspective, alternative delivery routes have been progressively tested and emphasized over the years either for AD or PD patients, including Transbuccal Drug Delivery Systems (TDDSs). Indeed, TDDSs represent a group of novel, different techniques to convey drugs through the oral mucosa both at the sublingual and genial level, theoretically overcoming the main bias of conventional oral assumption.  
This review aims to provide an overview of the main TDDSs that are available, or in development, for AD and PD patients. Moreover, we highlight the relevance of oral health in patients with neurodegenerative disease, as an essential condition to successfully approach such a novel kind of therapy [21; 22; 23; 24].