What is Parkinson's disease

It is difficult to claim that we really know exactly what Parkinson's Disease (PD) actually is, apart from the fact that it impacts the brain (and many other parts of the body), and is a progressively degenerative disease.
We do not know for sure what causes PD.
We cannot currently cure PD.
We do however know what the presenting symptoms of PD look like, and we can mitigate a number of these symptoms (to some degree) for a period of time.
We can also see (at least some of) the irregular occurences in the body, which accompany PD symptoms.
We can only speculate at this stage as to how and why these irregularities develop.
In short, we do not know the exact inter-relationships of all these observable phenomena (and there are probably more we have yet to discover).
So, for now, let us identify some of the things we do know about Parkinson's Disease: 
(1) PD is a progressive disease that can be fatal, usually over an extended period of many years. (It is not a "fast" disease like certain versions of ALS, although it does on average, moderately decrease the patient's average life expectancy. In a small percentage (<5%) of cases, for reasons we do not understand, it may never lead to significant impairment.)
The main impact of PD is normally a progressive and severe reduction in quality of life, precipitated by the gradual degradation of a variety of bodily and mental functions.
The average onset age is 63 ... but very rare "young onset" cases may be diagnosed as early as childhood or adolesence. 
(2) PD gradually destroys the ability to move, by killing off the dopamine producing neurons in a part of the brain called the substantia nigra. We can see the disappearance of these dopamine producing neurons clearly with DaTscan technology, which qualifies PD to be classified as a "neuro-degenerative" disease, since it destroys brain neurons.
Dopamine is essential for transmitting movement instructions - both voluntary (walking, smiling etc.) and involuntary (breathing, digestion etc.) - from the substantia nigra to a part of the brain called the striatum (which plays a key part in managing movement). So, when you decide to move your arm or leg, the motor centers of your brain notify the striatum which is responsible for adjusting the tone (force and speed) of the muscles involved in that particular movement to make it smooth and precise. The striatum collects vast amounts of data (from eyes, ears, muscles, object locations etc.) to compute the desired movement outcome. The substantia nigra neurons then use dopamine to adjust the 'level of receptiveness' of the striatum's neurons to "fine-tune" their level of excitedness via a "push-pull" process to produce smooth and controlled movements. Take away some of the dopamine that facilitates this 'inter-neuron dialogue' and the result is PD style movement. (An automobile analogy might be a partial transmission failure which results in driving with the breaks on.)    
(3) PD has some connection (in differing degrees) to mutations occuring in over 25 of our roughly 2,500 genes. This number continues to rise as genetic research advances. The most common gene mutations in PD Patients occur on the LRRK2 gene, but even this only accounts for about 2% of all PD cases. In short, genetic mutations, so far as we know at present, only account for about 10% of PD cases.
(4) PD produces a wide variety of symptoms which generally include tremor, rigidity, slowness in movement. A wide variety of other symptoms develop over time such as weak voice, small hand writing, swallowing difficulties, insomnia, dystonia, constipation, significant loss of muscle strength, "freezing" of movement, fatique, dementia and depression. 
(5) Movement difficulty and "freezing" responds reasonably well to treatment with levodopa, which is ingested and absorbed in the first few centimeters of the intestine immediately below the stomach. In the brain the ingested levodopa is converted to dopamine, which improves movement capabilities.  Getting the levodopa across the blood-brain barrier has so far not been achieved by any other FDA approved methodology, although clinical trials using inhaled levodopa are close to FDA approval. The downside of consuming levodopa is that some of it remains in the the body's peripheral nervous system and causes dyskinesia (wild, jerky, uncontrollable limb and body motions). There is a relationship between the duration of levodopa consumption and the enhancement of dyskinesia. Dyskinesia appears to non-reversible even if the ingestion of levodpa is discontinued. Dyskinesia is somewhat treatable with Amantadine (a FDA approved anti-viral drug which is also approved PD), and DBS (Deep Brain Stimulation via surgically implanted electrodes in the brain stem).
(6) Historically, whenever researchers disected the brain tissue of deceased PD Patients, they all contained accumulations of a protein called alpha-synuclein. Astonishingly, in 2013, we discovered via new research that this was NOT true for PD patients who carried mutations on the PARK2 gene (a small % of PD patients often associated with "young onset" of PD (prior to 50 years), and also do NOT develop dementia.) Alpha-synuclein is widely used in the brain, although its "normal" function is not known. These 'globs' or accumulations of alpha-synuclein are called "Lewy-Bodies". Alpha-synuclein aggregations have also been found in PD patient's spinal columns, and even the colon. Lewy bodies also contain another protein called ubiquitin, which has links to some other hereditary forms of PD. Ubiquitin seems to have a role in removing old proteins from inside neurons, so any mutations which impair a 'take out the rubbish function' would help explain these accumulations of old proteins. This 2013 discovery throws the central theory (that alpha-synuclein accumulations somehow kill of dopamine producing neurons) into question. Are we looking at two different diseases that present the same way ? Or, is our model so flawed that we are missing a key bit of information which prevents us from really understanding PD at all ?                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
(7) There is a gene responsible for alpha-synuclein production which is known as the alpha-synuclein gene (code is SNCA) and at least 18 mutations of this gene have been identified so far. However mutations in the SNCA gene are extremely rare in PD patients, only occuring mostly in patients of Greek and Italian origin. (The most common gene mutations in PD patients involve the LRRK2 gene.)
These anomalies have led most PD Researchers to believe that "environmental trigger(s)" are also involved in the onset of PD, and pesticides and herbacides are amongst the primary suspects. The first real scientific support for this theory came in  February 2014 when scientists at the University of California, Los Angeles linked pesticides which inhibited the production of aldehyde dehydrogenase (ALDH) to PD. They also found that mutations on the ALDH2 gene carried a hugely increased PD risk, but only when coupled with exposure to these pesticides. (see RESEARCH & NEWS tab on this website for details; "How pesticides can boost PD risks") 
(8) PD occurs around the world and affects 6+ million people. Japan is the only country where the incidence of PD in woman clearly exceeds the incidence in men (although some studies include Russia, Netherlans and Italy). Globally women only account for about one third of PD cases.
(9)  Slowing the progression of PD with exercise, is emerging as one of the key weapons in fighting the progression of PD. Cardio-vascular exercises produce enhanced blood flow and elevated metabolic rates which may assist failing "trash removal" brain functions designed to remove or disassemble old proteins, malfunctioning mitochondria or defective neurons.