Synaptic Dysfunction in Parkinson's Disease

Overview

Synaptic dysfunction represents one of the earliest and most critical pathological features of Parkinson’s disease](/diseases/parkinsons-disease) (Parkinson’s disease), preceding dopaminergic neurons loss and motor manifestations by years or even decades^{1Clinical progression of Parkinson's disease and the neurobiology of axons2010 · Ann Neurol · PMID 20518033Open reference}. The synapse, the fundamental unit of neurons communication, relies on precisely coordinated processes including neurotransmitter synthesis, vesicle trafficking, release, and recycling. In Parkinson’s disease, these intricate mechanisms become disrupted through multiple interconnected pathways, including alpha-synuclein pathology, mitochondrial dysfunction, lysosomal impairment, and neuroinflammation[^2. Understanding synaptic dysfunction provides crucial insights into disease progression and offers therapeutic targets for disease-modifying interventions.

Pathway / Mechanism Diagram

graph TD
    A["Abeta Oligomers / Tau / alpha-Synuclein"] --> B["Postsynaptic Receptor Disruption"]
    A --> C["Presynaptic Vesicle Dysfunction"]
    B --> D["NMDAR Internalization"]
    B --> E["AMPAR Removal"]
    D --> F["Impaired LTP"]
    E --> F
    C --> G["Reduced Neurotransmitter Release"]
    G --> F
    F --> H["Dendritic Spine Loss"]
    A --> I["Complement-Mediated Synapse Elimination"]
    I --> J["Microglial Synapse Phagocytosis"]
    J --> H
    H --> K["Circuit Disconnection"]
    K --> L["Cognitive Decline"]
    style A fill:#ef5350,color:#e0e0e0
    style H fill:#5d4400,color:#e0e0e0
    style L fill:#ef5350,color:#e0e0e0

Molecular Architecture of the Synapse

Presynaptic Terminal Structure

The presynaptic terminal is a highly specialized compartment dedicated to neurotransmitter release. Dopaminergic neurons in the substantia nigra pars compacta (SNc) possess unique synaptic properties that make them particularly vulnerable to Parkinson’s disease-related insults^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}. The terminal contains synaptic vesicles organized in distinct pools: the readily releasable pool (RRP), the recycling pool, and the reserve pool. These vesicles undergo regulated exocytosis mediated by the SNARE complex, comprising syntaxin-1, SNAP-25, and synaptobrevin (VAMP2)^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}.

Dopamine Synthesis and Packaging

Dopamine synthesis occurs through a well-characterized enzymatic pathway beginning with tyrosine hydroxylase (TH), which converts tyrosine to L-DOPA, followed by aromatic L-amino acid decarboxylase (AAlzheimer’s diseaseC), which converts L-DOPA to dopamine^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}. The vesicular monoamine transporter 2 (VMAT2) packages dopamine into synaptic vesicles, protecting it from oxidative degradation and enabling regulated release. This compartmentalization is critical because cytosolic dopamine can undergo auto-oxidation, generating reactive oxygen species (ROS) that contribute to oxidative stress^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}.

Postsynaptic Receptor Architecture

Dopaminergic signaling is mediated primarily by two receptor families: D1-like receptors (D1, D5) that stimulate adenylyl cyclase, and D2-like receptors (D2, D3, D4) that inhibit it^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}. The basal ganglia express high levels of D1 and D2 receptors in distinct neurons populations—the direct pathway (D1-expressing) and indirect pathway (D2-expressing)—whose balanced activity is essential for normal motor control.

Mechanisms of Synaptic Dysfunction in Parkinson’s disease

Alpha-Synuclein-Induced Synaptic Impairment

Alpha-synuclein (αSyn), the protein that forms Lewy bodies in Parkinson’s disease, directly disrupts synaptic function through multiple mechanisms^{7'Synaptic dysfunction in Parkinson''s disease: from alpha-synuclein pathology to synaptic protein loss'2020 · Prog Neuropsychopharmacol Biol Psychiatry · PMID 32143583Open reference}. In its monomeric form, αSyn localizes to presynaptic terminals where it regulates vesicle trafficking and neurotransmitter release. However, in Parkinson’s disease, αSyn undergoes aggregation into oligomers and fibrils that become toxic to synapses^{8Alpha-synuclein toxicity in neurodegeneration2017 · Nat Med · DOI 10.1038/nm.4269Open reference}.

Research demonstrates that αSyn oligomers specifically bind to synaptic vesicles, impairing their ability to release neurotransmitter^{9Alpha-synuclein oligomers bind to synaptic vesicles and inhibit neurotransmitter release2017 · J Biol Chem · PMID 28302766Open reference}. Studies using patient-derived neurons show that αSyn accumulation leads to reduced synaptic vesicle density, impaired vesicle recycling, and decreased neurotransmitter release probability^{10The synaptic pathology of alpha-synuclein aggregation in Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy2010 · Acta Neuropathol · PMID 20610298Open reference}. The prion-like propagation of αSyn pathology to anatomically connected neurons explains the progressive spread of synaptic dysfunction throughout the nigrostriatal system^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}0.

Oligomer-Induced Channel Dysfunction

αSyn oligomers directly interact with synaptic ion channels, causing aberrant channel activity. In particular, voltage-gated calcium channels become dysregulated, leading to excessive calcium influx during synaptic activity^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}1. This calcium dysregulation triggers downstream toxic pathways including calpain activation and mitochondrial permeability transition. Studies show that αSyn oligomers form pore-like structures in synaptic membranes, causing membrane depolarization and neurotransmitter leak^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}2.

Synaptic Vesicle Depletion

Chronic αSyn pathology leads to progressive depletion of synaptic vesicle pools. The readily releasable pool (RRP) becomes particularly affected, with dramatic reductions in the number of fusion-competent vesicles^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}3. This depletion reflects both impaired vesicle recycling and reduced vesicle biogenesis. Ultrastructural studies of Parkinson’s disease brain tissue reveal fewer synaptic vesicles per terminal and abnormal vesicle morphology^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}4.

Presynaptic Terminal Remodeling

In response to αSyn accumulation, presynaptic terminals undergo structural remodeling. Synaptic active zones—the specialized regions where vesicle fusion occurs—become disorganized^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}5. Key active zone proteins including piccolo, bassoon, and rim1 show altered localization and expression. This structural disruption further impairs neurotransmitter release capacity.

Mitochondrial Dysfunction and Synaptic Energy Crisis

Synaptic activity is extraordinarily energy-intensive, requiring constant ATP generation to maintain ion gradients, vesicle cycling, and receptor function^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}6. Mitochondrial dysfunction in Parkinson’s disease compromises synaptic energy supply through several mechanisms. Mutations in PINK1 and PARKIN, causal in familial Parkinson’s disease, impair mitophagy—the process by which damaged mitochondria are selectively eliminated^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}7. Accumulation of defective mitochondria in synaptic terminals leads to ATP depletion, calcium dysregulation, and increased ROS production^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}8.

Studies in mouse models with mitochondrial complex I inhibition (mimicking Parkinson’s disease pathology) demonstrate dramatic synaptic deficits, including reduced spontaneous release, impaired vesicle replenishment, and altered short-term plasticity^{2Neuronal vulnerability, pathogenesis, and Parkinson's disease2013 · Mov Disord · PMID 23408227Open reference}9. Human neuroimaging studies using PET with mitochondrial complex I substrates confirm decreased synaptic energy metabolism in the basal ganglia of Parkinson’s disease patients^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}0.

Lysosomal Dysfunction and Synaptic Protein Degradation

The lysosomal-autophagy system is essential for synaptic protein turnover and organelle quality control^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}1. Lysosomal dysfunction, observed in most Parkinson’s disease cases due to GBA mutations, ATP13A2 deficiency, or other factors, impairs the degradation of αSyn and other aggregation-prone proteins^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}2. This leads to their accumulation in synaptic terminals, where they interfere with normal synaptic function.

Autophagic flux impairment in dopaminergic neurons results in the accumulation of damaged organelles, including mitochondria and lysosomes themselves, within synaptic terminals^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}3. The resulting proteostatic stress compromises the synaptic vesicle cycle and neurotransmitter release machinery.

Calcium Dysregulation and Synaptic Exhaustion

Dopaminergic neurons exhibit rhythmic pacemaking activity that relies on L-type calcium channels^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}4. This calcium influx, necessary for sustained firing, becomes dysregulated in Parkinson’s disease due to αSyn-mediated channel dysfunction and mitochondrial impairment. Elevated cytosolic calcium accelerates mitochondrial ROS production and depletes ATP reserves^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}5.

Synaptic terminals are particularly vulnerable to calcium dysregulation because calcium triggers synaptic vesicle exocytosis and also activates calpains, calcium-dependent proteases that degrade synaptic proteins^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}6. Excessive calcium influx leads to synaptic protein cleavage and impaired neurotransmission.

Neuroinflammation and Synaptic Pruning

Microglial activation in Parkinson’s disease contributes to synaptic dysfunction through both direct and indirect mechanisms. Activated microglia release pro-inflammatory cytokines including IL-1β, TNF-α, and IL-6, which directly impair synaptic function^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}7. These cytokines reduce synaptic vesicle release probability and alter postsynaptic receptor trafficking. Additionally, microglia phagocytose synaptic material in a process termed “synaptic pruning,” which is enhanced in the inflamed Parkinson’s disease brain^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}8.

Complement system activation plays a key role in inflammation-mediated synaptic loss. C1q and C3 tagging of synapses targets them for microglial elimination^{3Molecular machines governing neurotransmitter release2018 · Nature · DOI 10.1038/s41586-018-0255-3Open reference}9. Studies in Parkinson’s disease models show increased complement deposition on dopaminergic synapses, correlating with synaptic loss severity^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}0.

Astroglial Contributions to Synaptic Dysfunction

Astrocytes play essential roles in synaptic maintenance, including neurotransmitter clearance, metabolic support, and ion homeostasis. In Parkinson’s disease, astrocyte dysfunction contributes to synaptic impairment through multiple mechanisms^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}1. Reduced glutamate uptake leads to extrasynaptic glutamate accumulation and excitotoxicity. Impaired potassium buffering disrupts neurons resting membrane potentials. Altered astrocytic metabolism reduces lactate supply to neurons, compromising synaptic energy requirements.

Neurotransmitter-Specific Deficits

Dopamine Release Impairment

In Parkinson’s disease, striatal dopamine release is dramatically reduced due to the progressive loss of nigral neurons. However, synaptic dysfunction precedes terminal loss, with studies demonstrating reduced dopamine release capacity in apparently intact neurons^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}2. This impairment involves:

1. Vesicular depletion: Reduced VMAT2 expression limits dopamine packaging^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}3

2. Release probability: Altered SNARE complex function reduces evoked release^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}4

3. Reuptake: Increased dopamine transporter (DAT) activity accelerates dopamine clearance^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}5

Glutamatergic Excitotoxicity

Excessive glutamatergic signaling contributes to synaptic dysfunction and neurons death in Parkinson’s disease^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}6. NMDA and AMPA receptor overactivation leads to excessive calcium influx, activating destructive enzymatic pathways. The subthalamic nucleus, a major glutamatergic output to the basal ganglia, becomes hyperactive in Parkinson’s disease, driving excitotoxic damage to dopaminergic neurons^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}7.

GABAergic Dysfunction

GABAergic transmission is altered in Parkinson’s disease, affecting both inhibitory and disinhibitory circuits^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}8. Reduced GABA release from interneurons contributes to excessive neurons firing and network dysfunction. GABAergic synapse loss correlates with cognitive impairment in Parkinson’s disease patients^{4'Pathophysiology of L-dopa-induced motor complications in Parkinson''s disease: recent advances'2019 · J Neural Transm · PMID 30852741Open reference}9.

Synaptic Dysfunction and Disease Progression

Preclinical Phase

Synaptic changes begin decades before clinical diagnosis. Studies in asymptomatic carriers of LRRK2 or GBA mutations show subtle synaptic alterations detectable by PET imaging of vesicular acetylcholine transporter (VAChT)^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}0. These early changes may represent compensatory mechanisms that eventually fail.

Early Clinical Phase

At diagnosis, approximately 50-70% of dopaminergic neurons have already been lost, with corresponding dramatic reductions in striatal dopamine release^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}1. However, remaining terminals show profound functional impairment beyond what can be explained by neurons loss alone. This indicates that synaptic dysfunction is a major contributor to clinical deficits.

Advanced Disease

In advanced Parkinson’s disease, extensive synaptic loss occurs throughout the basal ganglia and cortical circuits^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}2. This widespread synaptic degeneration explains the progressive development of motor complications (dyskinesias, freezing of gait) and non-motor symptoms (cognitive decline, autonomic dysfunction).

Diagnostic and Therapeutic Implications

Synaptic Biomarkers

Synaptic dysfunction can be assessed using PET imaging of presynaptic terminals. Radiotracers targeting VMAT2 (e.g., ^18F-FP-DTBZ) provide quantitative measures of dopaminergic terminal integrity^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}3. More recently, synaptic vesicle glycoprotein 2A (SV2A) PET ligands enable visualization of global synaptic loss^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}4.

Cerebrospinal fluid (CSF) biomarkers reflecting synaptic degeneration include neurogranin, SNAP-25, and synaptotagmin^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}5. These proteins are elevated in Parkinson’s disease and correlate with disease severity and progression.

Electrophysiological Biomarkers

Transcranial magnetic stimulation (TMS) provides non-invasive assessment of cortical synaptic function. Motor evoked potential (MEP) measurements reveal altered cortical excitability in Parkinson’s disease^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}6. Paired-pulse TMS protocols assess intracortical inhibition and facilitation, showing characteristic changes in Parkinson’s disease patients^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}7.

Therapeutic Strategies

Dopamine Replacement: Levodopa and dopamine agonists partially compensate for reduced synaptic dopamine but do not address underlying synaptic pathology^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}8. Long-term treatment leads to dyskinesias, partly due to non-physiological dopamine receptor stimulation.

Synaptic Function-Targeting Drugs: Several experimental approaches aim to restore synaptic function:

• Alpha-synuclein aggregation inhibitors: Reduce toxic oligomer formation^{5'Dopamine neurons death in Parkinson''s disease: role of oxidative stress'2021 · Antioxid Redox Signal · PMID 32799712Open reference}9

• Mitochondrial protectants: Coenzyme Q10, MitoQ improve synaptic energy metabolism^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}0

• Calcium channel blockers: Isradipine reduces calcium-induced synaptic stress^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}1

• Autophagy enhancers: Improve lysosomal clearance of toxic proteins^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}2

Gene Therapy: AAV-mediated expression of VMAT2, GAlzheimer’s disease, or aromatic L-amino acid decarboxylase aims to restore neurotransmitter synthesis and release^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}3.

Mouse Models of Synaptic Dysfunction

Genetic mouse models have provided critical insights into Parkinson’s disease-related synaptic dysfunction. Models using viral αSyn overexpression, A53T mutant expression, or knock-in of Parkinson’s disease-associated mutations demonstrate age-dependent synaptic deficits^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}4. Conditional models allowing temporal control show that synaptic dysfunction occurs rapidly after αSyn accumulation, before neurons loss^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}5.

MitoPark mice, with mitochondrial dysfunction restricted to dopaminergic neurons, exhibit progressive synaptic deficits resembling human Parkinson’s disease^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}6. These models enable testing of synaptic-restoring therapies before irreversible neurons loss occurs.

Comparative Analysis: Synaptic Dysfunction Across Neurodegeneration

Alzheimer’s Disease

While Alzheimer’s disease is primarily characterized by amyloid and tau pathology, synaptic dysfunction is the strongest correlate of cognitive impairment^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}7. Postsynaptic changes, particularly dendritic spine loss, predominate in Alzheimer’s disease, while presynaptic deficits are more prominent in Parkinson’s disease. This reflects the different proteinopathies underlying each disorder.

Amyotrophic Lateral Sclerosis

Motor neuron disease involves profound synaptic dysfunction at the neuromuscular junction and central synapses^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}8. Unlike Parkinson’s disease, where dopaminergic terminals are primarily affected, Amyotrophic lateral sclerosis shows widespread synaptic loss affecting excitatory and inhibitory circuits.

Dementia with Lewy Bodies

DLB shares αSyn pathology with Parkinson’s disease but shows more prominent cortical synaptic loss, correlating with cognitive fluctuations and visual hallucinations^{6'Dopamine receptors: from structure to function'1998 · Physiol Rev · PMID 9457173Open reference}9. The distribution of synaptic pathology distinguishes Parkinson’s disease dementia from DLB.

Future Directions

Single-Cell Synaptic Analysis

Emerging technologies enabling synaptic proteomics and transcriptomics from individual neurons will reveal cell-type-specific vulnerability mechanisms^{7'Synaptic dysfunction in Parkinson''s disease: from alpha-synuclein pathology to synaptic protein loss'2020 · Prog Neuropsychopharmacol Biol Psychiatry · PMID 32143583Open reference}0. These approaches will identify novel therapeutic targets specific to vulnerable neurons populations.

Optogenetic Dissection

Optogenetic tools allow precise manipulation of synaptic activity in model systems^{7'Synaptic dysfunction in Parkinson''s disease: from alpha-synuclein pathology to synaptic protein loss'2020 · Prog Neuropsychopharmacol Biol Psychiatry · PMID 32143583Open reference}1. Combining channelrhodopsin with Parkinson’s disease-related genetic or pharmacologic insults enables mechanistic dissection of synaptic dysfunction.

Human Stem Cell Models

Patient-derived induced pluripotent stem cells (iPSCs) differentiated into dopaminergic neurons provide human disease models for synaptic studies^{7'Synaptic dysfunction in Parkinson''s disease: from alpha-synuclein pathology to synaptic protein loss'2020 · Prog Neuropsychopharmacol Biol Psychiatry · PMID 32143583Open reference}2. These models recapitulate patient-specific vulnerabilities and enable personalized therapeutic testing.

Conclusions

Synaptic dysfunction represents a central pathogenic mechanism in Parkinson’s disease, beginning early in disease course and contributing to both motor and non-motor manifestations. The multiple converging pathways—αSyn pathology, mitochondrial dysfunction, lysosomal impairment, calcium dysregulation, neuroinflammation, and astrocyte dysfunction—create a synergistic attack on synaptic integrity. Understanding these mechanisms provides crucial targets for disease-modifying therapies aimed at preserving synaptic function and preventing progressive neurodegeneration.

The preservation and restoration of synaptic function represents one of the most promising avenues for developing disease-modifying treatments for Parkinson’s disease. By targeting the earliest pathological events in Parkinson’s disease, therapeutic interventions may potentially slow or halt disease progression before irreversible neurons loss occurs.

See Also

• Parkinson’s disease

• Parkinson’s disease

• alpha-synuclein

• mitochondrial dysfunction

• neuroinflammation

• Alzheimer’s disease

• oxidative stress

• autophagy

• tau

• Amyotrophic lateral sclerosis

External Links

• PubMed

• KEGG Pathways