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The Universal Non-Neuronal 
Nature of Parkinson’s Disease:  
A Theory 

 
André X. C. N. Valente1,2,3, Altynai 
Adilbayeva4,Tursonjan Tokay4, 
Albert A. Rizvanov3 
 
1Center for Neuroscience and Cell 
Biology, University of Coimbra, 
Cantanhede, Portugal; 2Biocant - 
Biotechnology Innovation Center, 
Cantanhede, Portugal; 3Institute of 
Fundamental Medicine and Biology, 
Kazan Federal University, Kazan, Russia; 
4National Laboratory Astana, Nazarbayev 
University, Astana, Kazakhstan 

 
Vol. 4, No. 1 (2015)   |   ISSN 2166-7403 (online)  
DOI 10.5195/cajgh.2016.231 |   http://cajgh.pitt.edu 

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Abstract 

Parkinson's disease (PD) is one of the most common neurodegenerative disorders, yet the etiology of the majority of its cases 
remains unknown. In this manuscript, relevant published evidence is interpreted and integrated into a comprehensive hypothesis 
on the nature, origin, and inter-cellular mode of propagation of sporadic PD. We propose to characterize sporadic PD as a 
pathological deviation in the global gene expression program of a cell: the PD expression-state, or PD-state for short. A universal 
cell-generic state, the PD-state deviation would be particularly damaging in a neuronal context, ultimately leading to neuron 
death and the ensuing observed clinical signs. We review why ageing associated accumulated damage caused by oxidative stress 
in mitochondria could be the trigger for a primordial cell to shift to the PD-state. We propose that hematopoietic cells could be 
the first to acquire the PD-state, at hematopoiesis, from the disruption in reactive oxygen species homeostasis that arises with age 
in the hematopoietic stem-cell niche. We argue that cellular ageing is nevertheless unlikely to explain the shift to the PD-state of 
all the subsequently affected cells in a patient, thus indicating the existence of a distinct mechanism of cellular propagation of the 
PD-state. We highlight recently published findings on the inter-cellular exchange of mitochondrial DNA and the ability of 
mitochondrial DNA to modulate the cellular global gene expression state and propose this could form the basis for the inter-
cellular transmission of the PD-state. 

Keywords:Parkinson’s disease,  

 

The Universal Non-Neuronal Nature 
of Parkinson’s Disease:  
A Theory 

 
André X. C. N. Valente1,2,3, Altynai 
Adilbayeva4, Tursonjan Tokay4, 
Albert A. Rizvanov3 
 
1Center for Neuroscience and Cell Biology, 
University of Coimbra, Cantanhede, 
Portugal; 2Biocant - Biotechnology 
Innovation Center, Cantanhede, Portugal; 
3Institute of Fundamental Medicine and 
Biology, Kazan Federal University, Kazan, 
Russia; 4National Laboratory Astana, 
Nazarbayev University, Astana, Kazakhstan 

Research 

Parkinson’s disease (PD) is a common 
neurodegenerative disorder associated with old age. The 
number of worldwide affected individuals is estimated 
at 7 to 10 million.1 With population ageing, particularly 
in developing countries2, this number is expected to 
increase steeply in the upcoming decades. 
Unfortunately, there is currently no cure for PD, with 
available medications only providing symptomatic 
relief.3  

PD is a movement disorder clinically 
characterized by tremor, bradykinesia, rigidity, and 
postural instability.4 The motor dysfunctions are a direct 
consequence of the death of dopamine-producing 
neurons in the substantia nigra pars compacta region of 
the midbrain. Histologically, the most noticeable feature 
of PD are abnormal aggregates of proteins, called Lewy 
bodies and Lewy neurites, that appear in the cell body 

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and neurites of PD patient neurons. Their major 
constituent is the protein alpha-synuclein. 

Familial genetic linkage studies have 
unequivocally associated six genes with Mendelian 
inheritable forms of PD.4 Still, these individual gene 
mutations account for fewer than 10% of PD cases. 
They generally lead to juvenile or early onset PD 
(before 50 years of age). Naturally, genetics still 
impacts the risk of an individual acquiring non-
monogenic sporadic PD later in life. Over a dozen 
single nucleotide polymorphisms (SNPs) have been 
statistically linked with sporadic PD through genome-
wide association studies (GWASs).5,6 However, the 
differential risks associated with carrying these SNPs, 
although statistically significant, are mostly very small 
in absolute terms. Similarly, although some 
environmental factors, such as exposure to metals or 
pesticides, have been statistically linked with PD, the 
associations do not appear to be sufficiently widespread 
to explain beyond a minority of PD cases.7 Thus, the 
etiology of the over 90% of cases classified as sporadic 
PD remains undetermined. 

We briefly highlight some of the major theories 
being pursued regarding the nature of sporadic PD. 
Different aspects of these hypotheses will be presented 
in more detail as relevant, throughout the article. An 
overarching hypothesis on the etiology of sporadic PD 
is that it is triggered by an external agent. Pesticides and 
metals would be two candidate environmental agents, 
given their statistical association with PD.7 Another 
proposed factor suggested in the literature is a 
neurothropic pathogen, such as a virus8 or a prion-like 
protein.9 Entry into the organism could be via the 
peripheral olfactory system10 or via the gastrointestinal 
tract,11 two sites associated with early prodromal 
clinical symptoms of PD. These two sites have also 
been combined into a dual-hit hypothesis, centered on 
an external agent simultaneously entering the organism 
via the two routes.12 Whether with an initially external 
origin or endogenously generated, the theory that a 

misfolded, prion-like self-propagating form of alpha-
synuclein is responsible for the disease is another major 
hypothesis currently under investigation.9,13 More 
endogenous, aging-related perspectives of sporadic PD 
focus on the role of oxidative stress and mitochondrial 
damage, for which there is significant evidence in PD 
patients. 14,15 Finally, although the view of sporadic PD 
as an autoimmune disease is not typical, the aggravating 
contribution of the neuro-inflammatory response to the 
disease is commonly acknowledged.16,17  

Starting from the analysis of sporadic PD 
blood gene-expression data, we have previously argued 
that sporadic PD could have a hematopoietic origin.18 In 
the present article, we review and expand on this 
original hypothesis, placing it in the context of recent 
developments in both PD and the broader biological 
research. The article first addresses why sporadic PD 
may be a systemic, rather than solely neuronal, 
condition. Then, it discusses why inter-cellular 
propagation of the pathology may be involved, rather 
than the pathology being purely associated with cell 
ageing phenomena. In particular, we present the 
possibility that the disease transmission may be enabled 
by the inter-cellular exchange of the mitochondrial 
DNA. Finally, the article revisits our previously 
published hypothesis that the pathology may initially 
begin at hematopoiesis. 

 

The universal nature of the PD-state 

In this section, we argue for the systemic 
nature of sporadic PD. Our case is centered on the 
interpretation of recently published evidence obtained 
by applying induced pluripotent stem cell (iPSC) 
technology to PD research.19,20 Using iPSC techniques, 
conveniently collected cells from PD patients, such as 
skin fibroblasts, can be reverted to a pluripotent state 
and subsequently differentiated into dopaminergic 
neurons. We believe that early PD iPSC experimental 

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results support a fundamental re-evaluation of the nature 
of the sporadic non-monogenic form of the disease. 

We summarize the main observations from two 
of the published PD iPSC studies.19,20 In both studies, 
skin fibroblasts from sporadic PD patients (presuppose 
sporadic henceforth) were reprogrammed back into 
pluripotent stem cells, which were then differentiated 
into dopaminergic neurons. Sánchez-Danés et al.19 
reported that, in comparison with neurons derived from 
fibroblasts from disease-free controls, neurons 
originating in fibroblasts from PD patients consistently 
showed PD phenotype associated alterations. These 
included reduced numbers of neurites, more limited 
neurite arborizations, and increases in caspase-3 
activity, a marker for cell apoptosis. Woodard et al.20 
utilized neurons derived from fibroblasts of two 
monozygotic twins discordant for PD. Multiple 
alterations that can be linked with a PD phenotype were 
present exclusively in the fibroblasts derived from the 
PD twin. These included lower dopamine levels, an 
elevation of alpha-synuclein in neurites, a delay in the 
emergence of spontaneous action potentials, and an 
absence of synchronous neuronal activity. 

An epidemiological study by Tanner et al.21 
reported a mere 15.5% concordance of monozygotic 
twins in developing PD. An analogous study in Sweden 
published by Wirdefeldt et al.22 corroborated this result, 
placing the concordance rate at 11%. Thus, excluding 
the monogenic cases, heredity does not ensure the 
emergence of PD. Therefore, the consistent, regular 
emergence of a PD phenotype in neurons derived from 
fibroblasts from PD patients cannot be attributed to a 
PD favorable germline genetic background in the 
patients. The conclusion is that the disease must have 
been present in the skin fibroblasts from the patients. 
PD is thus a systemic condition, not confined to 
neuronal cells. 

We propose to characterize PD as a 
pathological deviation in the expression program of a 
cell: the PD expression-state, or PD-state for short.18,23 

Reports of a characteristic PD gene-expression signature 
across multiple tissues support this view.18,24-26 The 
recent observation of a unique, concordant pattern of 
methylation in post-mortem frontal cortex samples and 
peripheral blood leukocytes from PD patients27 
reinforces this standpoint, further suggesting that the 
PD-state may be stabilized by DNA epigenetic 
modifications. 

 

The role of ageing in PD 

In spite of possessing a multitude of self-repair 
mechanisms, all cells undergo the ageing process.28 
They gradually accumulate dysfunctional molecules, as 
well as random mutations and other assorted alterations 
in their genetic code, ultimately resulting in the ageing 
phenotype. As a source of free radicals, mitochondria 
and the mitochondrial DNA are particularly vulnerable 
to oxidative stress damage.29 This observation has led to 
the theory that the mitochondrial dysfunction caused by 
oxidative stress plays a central role in ageing.30,31 With 
PD arising at old age and with mitochondrial function 
specifically known to be compromised in a variety of 
cell types in PD patients,32-35 the mitochondrial theory 
of aging broadly views PD as yet another manifestation 
of this phenomenon.14  

It is conceivable that accumulated random 
damage, possibly in mitochondrial DNA and due to 
oxidative stress, eventually triggers the gene expression 
program of a cell to shift to the PD-state. This shift to 
the PD-state in a cell could thus be viewed as a 
probabilistic event, its likelihood being a (nonlinearly) 
increasing function of the accumulated damage. 
However, we argue that it is impossible for all the PD-
state cells in an affected individual to have acquired the 
PD-state in this fashion. 

The following valid scenario may be 
considered. Imagine two monozygotic twins, one 
diagnosed with PD in the past, with the other being 
disease-free at the present time. Let the unaffected twin 

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presently exhibit a greater amount of age accumulated 
damage than the affected twin did at the time of his PD 
diagnosis – this would be the case given enough years 
had elapsed since the original diagnosis. Now, assume 
that accumulated random damage is the only possible 
trigger of the PD-state in a cell. Then, the observed 
greater age accumulated damage in the undiagnosed 
twin at present would guarantee a currently greater 
probability for his or her individual cells to acquire the 
PD-state than that probability was for the cells of the 
affected twin at the time of his PD-diagnosis. Yet, the 
unaffected twin continues to show no clinical signs of 
PD at present, in contrast with the affected twin at the 
time of his PD diagnosis. Thus, assuming that 
accumulated random damage is the only possible trigger 
of the PD-state in a cell leads to a probabilistic paradox. 

We make two remarks on the argument 
presented in the previous paragraph. Firstly, 
accumulated random damage causing a cell to shift to 
the PD-state does not pose a paradox. Only the presence 
of most of the PD-state cells in the organism cannot be 
explained by such a process. Therefore, ageing-
associated damage, caused by oxidative stress in 
mitochondria, could still be the trigger for a primordial 
cell in the organism to shift to the PD-state. Secondly, 
ageing-associated cellular damage may not be required 
for the subsequent dissemination of the PD-state across 
the organism since, as argued, this dissemination would 
occur via a distinct mechanism. 

There are two direct pieces of evidence 
supporting a propagation dynamic in PD. First, analyses 
of post-mortem neuronal tissue from patients who died 
at different stages of the disease appear to support a 
chronological, physical spread of Lewy-bodies across 
the nervous system.36 Second, there is published 
evidence on the surgical transplantations of fetal ventral 
mesencephalic dopaminergic neurons as a treatment of 
PD. A number of post-mortem analyses, performed over 
10 years after the transplant, detected Lewy-bodies and 
Lewy neurites in grafted neurons, in spite of the still 

young age of the transplanted tissue.37,38 This latter fact 
is in addition evidence of the non-essentiality of cellular 
ageing to the acquisition of the PD-state. 

In this section, we argued that ageing-
associated damage caused by oxidative stress in 
mitochondria could be the trigger for a primordial 
individual cell to shift its gene expression program to 
the PD-state. The shift to the PD-state would be a 
probabilistic event, its likelihood increasing nonlinearly 
with that accumulated damage in the cell. On the other 
hand, the subsequent appearance of the PD-state in 
numerous other cells could no longer be explained by 
cell ageing. Rather, it likely involves a separate 
mechanism of propagation of the PD-state. 

 

The propagation of the PD-state 

The spread of the PD-state is a slow process, as 
evidenced by the approximate decade that it takes an 
implanted fetal neuron in the brain of a PD patient to 
develop Lewy bodies.37,38 The mechanism of 
propagation of the PD-state remains undetermined. 
However, new modes of inter-cellular communication 
continue to be discovered.39 In this section, we discuss 
how propagation of the PD-state may occur. 

One hypothesis posits that alpha-synuclein can 
behave as a prion and that PD is a prion disorder.9,13 
Under this theory, there exists a misfolded form of 
alpha-synuclein that is self-propagating, having the 
ability to induce similar misfolding in well-conformed 
alpha-synuclein. The transfer of the misfolded form of 
alpha-synuclein from cell to cell would thus result in the 
inter-cellular spread of PD. However, a western blot 
analysis did not detect any alpha-synuclein in the 
fibroblasts utilized in the PD iPSC experiments 
discussed earlier.20 Therefore, a PD phenotype in 
fibroblast-derived neurons cannot be explained by the 
lingering presence of a hypothetical infectious form of 
alpha-synuclein. 

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Nevertheless, there is the possibility that a 
different biological entity is responsible for propagating 
the PD-state. Recently, the inter-cellular exchange of 
mitochondrial DNA (mtDNA) has been 
demonstrated.40,41 We propose that mtDNA could be the 
vehicle for the inter-cellular transmission of the PD-
state. 

Comprehensive research with neuron-platelet 
cytoplasmic hybrids supports that anomalous mtDNA 
may suffice to set off the PD-state in a cell. A PD cybrid 
cell is created in vitro by the fusion of a neuronal cell 
depleted of endogenous mtDNA with an enucleated 
platelet from a PD donor. Thus, the mtDNA of the 
cybrid cell is that of the platelet from the PD patient, 
while its nuclear DNA is that of the disease-free 
neuronal cell. Various PD characteristic alterations have 
been observed in PD cybrids, most prominently, 
inclusions that replicate the essential biochemical and 
structural features found in Lewy-bodies in the brain of 
PD patients.15,42,43  

The sufficiency of mtDNA to trigger the PD-
state in a cell is supported by its ability to induce 
epigenetic modifications and to modulate gene-
expression in nuclear DNA. In the context of 
tumorigenesis, work by Smiraglia et al.44 and by Xie et 
al.45 shows that alterations to mtDNA affect the 
methylation pattern of various nuclear genes. Bellizzi et 
al.46 report that methylation and gene expression 
patterns of nuclear genes in cybrids depend on the 
mtDNA donor haplogroup. Kelly et al.47 proposed that 
mtDNA haplotypes play a pivotal role in the process of 
differentiation and mediate the fate of the cell. In mouse 
undifferentiated and differentiating embryonic stem 
cells, with the same nuclear DNA haplotype but distinct 
mtDNA haplotypes, they observed mtDNA haplotype-
specific expression of genes involved in pluripotency, 
differentiation, mitochondrial energy metabolism, and 
DNA methylation. 

No specific mutations in mtDNA have been 
consistently associated with PD.48 However, 

heteroplasmy of mtDNA (i.e., the presence of multiple 
mtDNA variants within a cell) is now widely 
appreciated.41 Thus, undetected lower frequency 
mtDNA variants could potentially be involved in the 
transmission of the PD-state. Additionally, the number 
of PD-state triggering variants could be too large for 
effective statistical detection. Alternatively, the PD-state 
could be a result of mtDNA epigenetic modifications. 
Whether mtDNA can be methylated is currently a 
matter of active debate.49,50 Hong et al.51 make a strong 
case for the absence of mtDNA methylation, at least 
under most biological conditions. On the other hand, a 
recent publication by Bacarelli et al.52 reports the 
presence of significant mtDNA methylation in platelets 
of cardiovascular disease patients. For instance, in 
sequenced sites in the MT-CO1 gene region, Bacarelli 
et al. report average percentage site methylation to be on 
the order of 25%.52 

 

A site of origin for the PD-state 

We have mentioned that ageing-associated 
damage caused by oxidative stress in mitochondria 
could be the trigger for a primordial cell to shift its gene 
expression program to the PD-state. The next relevant 
question is: Where would an initial PD-state cell most 
commonly arise? In this section, we suggest the 
hematopoietic stem cell niche as a site to consider. 

Research based on gene expression,18,25 DNA 
methylation,27 neuron-platelet cybrid,15,42,43 and 
bioenergetic33 analyses supports the presence of the PD-
state in circulating hematopoietic cells. Given the short 
lifespan of blood cells (days for platelets53 and 
granulocytes54 and weeks for lymphocytes, with the 
exception of memory cells55) by comparison with the 
decade long timescale for the transmission of PD across 
the neuronal system,36-38 the above signs of  PD in blood 
point to circulating hematopoietic cells acquiring the 
PD-state at hematopoiesis, rather than after maturation. 

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Hematopoiesis is altered with ageing. In terms 
of global gene expression in hematopoietic stem cells 
(HSCs), nitric oxide mediated signal transduction, the 
NF-kB cascade and the pro-inflammatory response are 
the most age up-regulated processes, while chromatin 
silencing, single-strand break repair, SMAD protein 
nuclear translocation and chromatin remodeling are the 
most down-regulated ones.56 Alterations at the HSC 
epigenetic level are supported by many chromosomal 
regions showing a coordinated change in transcriptional 
activity.56 Fate-wise, a skewing to the myeloid line and 
a diminished lymphoid potential are observed with 
ageing.57  

It has been known for a long time that reactive 
oxygen species (ROS), if not properly checked, have the 
potential to cause indiscriminate cellular damage.30 
Today, it is recognized that ROS may also play a 
functional signaling role in activating processes such as 
the inflammatory and stress responses.28,58 Additionally, 
there is indication that ROS play a role in regulating 
hematopoiesis.59 In particular, evidence associates 
abnormal ROS levels at old age with a dysfunction in 
both the proliferation and the differentiation dynamics 
of HSCs. In vitro research has shown that exposure to 
H2O2 can lead to chromosomal translocations in 
HSCs.60 Ionizing radiation is also known to affect 
HSCs, as it has been found to promote differentiation, 
short-term apoptosis and long-term senescence of 
HSCs.61 Work with Drosophila supports the role of ROS 
in the regulation of hematopoietic cell fate. Increasing 
ROS beyond its basal level in Drosophila multipotent 
hematopoietic progenitor cells triggers their precocious 
differentiation.62 Conversely, scavenging ROS from 
these hematopoietic progenitors retards their 
differentiation into mature blood cells.62 It is well-
established that serial transplantation of human HSCs 
into immunodeficient mice leads to both elevated 
intracellular ROS levels and to premature HSC 
senescence.63-65 Yahata et al.63 and Ito et al.65 
independently reported that antioxidant pharmacological 
inhibition of ROS can mitigate this deteriorating HSC 

phenotype. Caloric restriction in BalbC mice was 
similarly shown to postpone HSC senescence.64 Finally, 
the same protective effect was achieved by SIRT3 up-
regulation in HSCs.66 HSCs are highly-enriched in this 
mammalian sirtuin, except for its suppressionat old 
age.66 SIRT3 regulates the global acetylation landscape 
of mitochondrial proteins and reduces oxidative stress.66 
Mechanistically, the FoxO transcription factors67 and the 
p53,68 Akt,69 MAPK,65 and ATM70 pathways have all 
been implicated in the ROS modulation of 
hematopoiesis. 

At the genetic level, emerging evidence may 
also connect PD and the hematopoietic system, although 
its interpretation is not yet completely clear. A new 
study by Xiao et al.71 found hematologic abnormalities 
in alpha-synuclein knock-out mice indicative of a role 
of alpha-synuclein in late-stage hematopoiesis. A 
genome-wide association study found that a rare non-
synonymous mutation in DZIP1 is a risk factor for PD.72 
DZIP1 is a component of the Hedgehog signaling 
pathway.73 Besides its role in directing embryonic 
pattern formation, the hedgehog pathway has been 
implicated in the maintenance of adult stem cell niches, 
including both neuronal74 and hematopoietic stem-
cells.75 Finally, PD patients are over five times more 
likely to be carriers of the mutated form of GBA 
responsible for the Gaucher's autosomal recessive 
disease.76 Gaucher's disease is characterized by low 
blood platelet levels, anemia, and the accumulation of 
the glycolipid glucocerebroside in the mononuclear 
phagocyte system.77  

In summary, we argued for the hematopoietic 
stem cell niche as a possible site for the appearance of a 
primordial PD-state cell based on evidence that 
supports: i) PD patients consistently having circulating 
hematopoietic cells in the PD-state; ii) Those 
hematopoietic cells more plausibly having acquired the 
PD-state at hematopoiesis, rather than after maturation; 
and iii) The critical role of ROS in regulating the 

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hematopoietic niche and the disruption of this 
homeostasis with ageing.  

 

Conclusion 

Based on recently published findings that we 
considered relevant to the PD field, as well as on 
various established lines of PD research, we presented a 
comprehensive theory on the nature, origin, and inter-
cellular mode of propagation of sporadic Parkinson's 
disease. We propose to define PD as a characteristic 
pathological deviation in the global gene expression 
program of a cell: the PD expression-state, or PD-state 
for short. Most significantly, we argue that any cell 
could be in the PD-state. However, due to the cell 
processes it affects the most, the PD-state deviation 
would be particularly damaging to neurons, ultimately 
leading to neuron death and the clinical manifestations 
of PD. 

Ageing-associated accumulated damage caused 
by oxidative stress in mitochondria could be the trigger 
for a primordial cell to shift to the PD-state. In 
particular, hematopoietic cells could be the first to 
acquire the PD-state, at hematopoiesis, as a result of the 
disruption in ROS homeostasis that arises with age in 
the hematopoietic stem-cell niche. The small correlation 
of PD incidence with genetic and environmental factors 
would mostly follow from this PD initiation dynamics. 

Propagation of the PD-state across the 
organism would occur in a second phase and via a 
distinct mechanism. We proposed that the ability of 
mtDNA to move across cells and to modulate the 
cellular global gene expression state could form the 
basis for this inter-cellular propagation of the PD-state. 
The mtDNA-based PD propagation dynamics would 
occur on a time-scale of years, as observed in patients, 
and not be ageing-dependent, in contrast with the PD 
initiation dynamics. 

Under physiological conditions, mice are not 
susceptible to PD late in life, in spite of clearly showing 
an ageing phenotype just as humans do.78 This absence 
of a PD phenotype in mice could thus more likely 
follow from the ageing-independent PD spread 
dynamics, than from the ageing-associated PD initiation 
dynamics. Namely, going from human to mouse, the 
mtDNA propagation dynamics would not scale 
appropriately time-wise to permit the condition to reach 
the neuronal system in the lifetime of a mouse. 

Early symptoms of PD in humans include 
impaired sense of smell10 and gastrointestinal 
dysfunction.79 Both have been reported as much as a 
decade before the appearance of symptoms at the motor 
level. They are typically interpreted as supporting the 
role of an external agent - entering via the olfactory or 
gastro-intestinal entry points - in inducting PD.12 
However, another characteristic shared by the olfactory 
bulb and the gastro-intestinal tract is that they are both 
sites of very active stem-cell based tissue 
regeneration.80,81 The rapid cell renewal and the 
plasticity of immature cells could facilitate both the 
cellular uptake of carriers of external mtDNA and the 
global cellular reprogramming to the PD-state, 
explaining the olfactory bulb and the gastro-intestinal 
tract being some of the earlier sites to which the PD-
state would spread. 

Finally, although our theory was presented in 
the context of PD, we note its general potential 
relevance to other pathologies where systemic 
bioenergetic cellular deficiency is a prominent feature. 

 

Acknowledgements 

The authors would like to thank the Montepio 
Foundation for financial support; the Center for 
Neuroscience and Cell Biology (project PEst-
C/SAU/LA0001/2013-2014); the Portuguese national 
funds via the programs FEDER and COMPETE; the 
Fundação para a Ciência e Tecnologia; the Program of 

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	The Universal Non-Neuronal Nature of Parkinson’s Disease:
	A Theory
	Abstract
	Keywords:Parkinson’s disease,
	The Universal Non-Neuronal Nature of Parkinson’s Disease:
	A Theory
	Research

