KIF28P — Kinesin Family Member 28, Pseudogene

KIF28P — Kinesin Family Member 28, Pseudogene

Overview

KIF28P (Kinesin Family Member 28, Pseudogene) is a pseudogene located on chromosome 3q29 that shares homology with the functional kinesin family genes[@miki2001]. While classified as a pseudogene, it provides important insights into the evolution of the kinesin superfamily and their roles in intracellular transport.

<div class="infobox infobox-gene">

| Property | Value |
|----------|-------|
| Gene Symbol | KIF28P |
| Full Name | Kinesin Family Member 28, Pseudogene |
| Chromosomal Location | 3q29 |
| NCBI Gene ID | 100130 |
| Ensembl ID | ENSG00000240445 |
| Gene Type | Pseudogene |
| Associated Diseases | None known |

</div>

Background

KIF28P is annotated as a pseudogene, meaning it bears sequence similarity to functional genes but contains mutations that prevent protein coding. However, pseudogenes can still play important roles in gene regulation through various mechanisms:

• Competitive endogenous RNA (ceRNA): Pseudogene transcripts can absorb microRNAs
• Gene conversion: Can serve as templates for gene correction
• Evolutionary remnants: Provide insights into gene family evolution[@poliseno2010]

Relationship to KIF28A

KIF28P is related to the functional gene KIF28A (Kinesin Family Member 28A):

...

KIF28P — Kinesin Family Member 28, Pseudogene

Overview

KIF28P (Kinesin Family Member 28, Pseudogene) is a pseudogene located on chromosome 3q29 that shares homology with the functional kinesin family genes[@miki2001]. While classified as a pseudogene, it provides important insights into the evolution of the kinesin superfamily and their roles in intracellular transport.

<div class="infobox infobox-gene">

| Property | Value |
|----------|-------|
| Gene Symbol | KIF28P |
| Full Name | Kinesin Family Member 28, Pseudogene |
| Chromosomal Location | 3q29 |
| NCBI Gene ID | 100130 |
| Ensembl ID | ENSG00000240445 |
| Gene Type | Pseudogene |
| Associated Diseases | None known |

</div>

Background

KIF28P is annotated as a pseudogene, meaning it bears sequence similarity to functional genes but contains mutations that prevent protein coding. However, pseudogenes can still play important roles in gene regulation through various mechanisms:

• Competitive endogenous RNA (ceRNA): Pseudogene transcripts can absorb microRNAs
• Gene conversion: Can serve as templates for gene correction
• Evolutionary remnants: Provide insights into gene family evolution[@poliseno2010]

Relationship to KIF28A

KIF28P is related to the functional gene KIF28A (Kinesin Family Member 28A):

• KIF28A: A functional kinesin motor protein involved in intracellular transport
• Chromosomal location: KIF28A is located on chromosome 2q37.3
• Function: May be involved in organelle transport and cell division
• Expression: Primarily expressed in testis and some brain regions

The presence of KIF28P suggests either:

Retrotransposition of a KIF28 ancestor gene

Duplication followed by pseudogenization

Ancient gene duplication event[@lawrence1997]

Kinesin Family Overview

The kinesin superfamily proteins (KIFs) are motor proteins that transport cargo along microtubules:

Classes of Kinesins

• Kinesin-1 (KIF5): Traditional kinesin, anterograde axonal transport
• Kinesin-2: Heterotrimeric, intraflagellar transport
• Kinesin-3: Monomeric, synaptic vesicle transport
• Kinesin-14 (KIFC): Minus-end directed

Roles in Neurodegeneration

Kinesin dysfunction is implicated in several neurodegenerative diseases:

• Alzheimer's Disease: Impaired axonal transport of [APP](/entities/app-protein) and [tau](/proteins/tau)
• Parkinson's Disease: Dysfunction in dopaminergic neuron transport
• Huntington's Disease: Defective transport of [huntingtin protein](/proteins/huntingtin)
• ALS: Disrupted mitochondrial and vesicle transport[@mandelkow2002]

Mitochondrial Transport in Neurodegeneration

Mitochondrial Dynamics in Neurons

Neurons require precise mitochondrial positioning:

• Synaptic terminals: High energy demand for neurotransmitter release
• Axonal branch points: Critical for calcium buffering
• Dendritic spines: Support local protein synthesis
• Initial segments: Ion channel clustering

Kinesin-1 (KIF5) mediates mitochondrial transport via the Milton-Miro complex:

• Milton (TRAK1/2): Adaptor protein connecting mitochondria to kinesin
• Miro1/Miro2 (RRHO1/2): Rho GTPases regulating mitochondrial transport
• Calcium sensing: Miro detects elevated Ca2+ and halts transport
• Motor switching: Miro can switch from kinesin to dynein for retrograde transport

Transport Defects in Neurodegeneration

Mitochondrial transport is particularly vulnerable:

Alzheimer's Disease:

• Tau pathology disrupts Milton-Miro complex function
• Reduced mitochondrial delivery to synapses
• Energy deficits contribute to synaptic failure
• Amyloid-beta impairs mitochondrial trafficking

Parkinson's Disease:

• Alpha-synuclein oligomers disrupt transport machinery
• PINK1/Parkin mitophagy pathway deficits
• Reduced mitochondrial support for dopaminergic neurons
• Increased mitochondrial calcium sensitivity

Amyotrophic Lateral Sclerosis:

• TDP-43 pathology disrupts RNA granule transport
• Mitochondrial transport severely impaired
• Energy deficits in motor neurons
• Axonal degeneration precedes cell body loss

Therapeutic Targeting

Restoring mitochondrial transport is a promising strategy:

• Miro1 modulators: Enhance mitochondrial motility
• Milton agonists: Improve kinesin-mitochondria coupling
• Calcium modulators: Reduce transport-inhibiting calcium spikes
• Mitochondrial biogenesis enhancers: Increase overall mitochondrial numbers

Synaptic Vesicle Transport

Synaptic Vesicle Lifecycle

Synaptic vesicles require constant delivery:

Synthesis: Vesicle proteins synthesized in soma

Transport: Kinesin-3 (KIF1A) mediates delivery to terminals

Loading: neurotransmitters packed into vesicles

Release: Exocytosis at active zones

Recycling: Endocytosis and re-loading

Kinesin-3 in Synaptic Function

KIF1A and related kinesin-3 motors are specialized for vesicle transport:

• Processive movement: Long runs without detaching
• Monovalent: Single motor can transport cargo
• Synaptic targeting: Enriched at presynaptic terminals
• Regulated activation: Phosphorylation-dependent activation

Mutations in KIF1A cause:

• Hereditary spastic paraplegia
• Intellectual disability
• Peripheral neuropathy
• Autism spectrum disorders

Transport in Disease Context

Synaptic vesicle transport deficits contribute to:

• Cognitive decline: Reduced neurotransmitter release
• Seizure susceptibility: Impaired inhibitory transmission
• Sleep disorders: Dysregulated synaptic function
• Motor deficits: Neuromuscular junction dysfunction

Axonal Transport Imaging and Analysis

Live-Cell Imaging Techniques

Advanced methods visualize transport:

• Fluorescent protein tagging: GFP-labeled cargo
• Total internal reflection microscopy (TIRF): Single-molecule resolution
• Fluorescence recovery after photobleaching (FRAP): Measure transport rates
• Kymography: Track individual movement events
• Super-resolution STED: Nanoscale transport visualization

Quantitative Measures

Key transport parameters include:

| Parameter | Normal | AD | PD |
|-----------|--------|----|----|
| Anterograde velocity | 0.5-1.0 μm/s | Reduced 40% | Reduced 30% |
| Retrograde velocity | 0.5-1.0 μm/s | Reduced 30% | Reduced 50% |
| Run length | 2-5 μm | Reduced 60% | Reduced 40% |
| Pause frequency | 5-10% | Increased 3x | Increased 2x |

Clinical Translation

Transport measurements could serve as biomarkers:

• Patient fibroblasts: Accessible cell type
• iPSC-derived neurons: Disease-relevant model
• Functional assays: High-throughput screening
• Longitudinal tracking: Monitor disease progression

Future Research Directions

Emerging Technologies

Future studies will employ:

• CRISPR screening: Identify transport-modifying genes
• Single-cell RNAseq: Profile transport-deficient neurons
• Organoid models: 3D neurodegeneration models
• Bioengineered scaffolds: Test therapeutic compounds

Key Research Questions

Outstanding questions include:

What determines selective neuronal vulnerability to transport defects?

Can transport be restored after prolonged dysfunction?

How do multiple transport pathways interact in disease?

What is the sequence of events in transport failure?

Can transport biomarkers predict clinical progression?

Therapeutic Outlook

The future of transport-targeted therapy looks promising:

• Combination approaches: Target multiple transport pathways
• Personalized medicine: Genotype-specific interventions
• Early intervention: Treat before irreversible damage
• Gene therapy: Deliver functional motor proteins
• Small molecule development: Brain-penetrant transport enhancers

Kinesin Superfamily in Neurodegeneration

Axonal Transport Mechanisms

Neurons rely on kinesin-mediated axonal transport to maintain synaptic function and cellular homeostasis. This process involves:

• Anterograde transport: Movement from cell body to synaptic terminals via kinesin motors
• Retrograde transport: Return of cargo to cell body via dynein motors
• Cargo types: Synaptic vesicles, mitochondria, proteins, RNA granules, endosomes

The microtubule cytoskeleton forms the tracks for this transport, with kinesin "walking" along microtubule filaments using ATP hydrolysis for energy[@stamer2002].

Kinesin Dysfunction in Alzheimer's Disease

In Alzheimer's disease, several mechanisms impair kinesin-mediated transport:

Tau pathology: Hyperphosphorylated tau accumulates in neuropil threads and neurofibrillary tangles, destabilizing microtubules and impairing transport[@dahl2010]

APP processing: Amyloid precursor protein trafficking is disrupted, affecting synaptic function

mitochondrial transport: Energy deficits impair mitochondrial delivery to synapses

Synaptic vesicle depletion: Reduced transport leads to neurotransmitter depletion

Studies show that kinesin-1 mediated transport is particularly vulnerable to tau-induced disruption, as tau competes with kinesin light chain for microtubule binding sites[@morfini2009].

Kinesin Dysfunction in Parkinson's Disease

Parkinson's disease involves selective vulnerability of dopaminergic neurons, with transport deficits playing a key role:

• Synaptic dysfunction: Impaired vesicle transport reduces dopamine release
• Mitochondrial dysfunction: Reduced mitochondrial transport leads to energy deficits
• Alpha-synuclein pathology: Lewy bodies disrupt axonal transport machinery
• Protein aggregation: Impairs motor protein function and cargo delivery

Research in experimental Parkinson models demonstrates that kinesin dysfunction precedes dopaminergic neuron death[@gunay2019].

Hereditary Neuropathies and Kinesin Mutations

Several hereditary neurological disorders result from kinesin mutations:

• Hereditary spastic paraplegia (HSP): Mutations in KIF1A, KIF5A genes cause axonal transport deficits[@takamura2022]
• Charcot-Marie-Tooth disease: Kinesin mutations contribute to peripheral neuropathy
• Intellectual disability: KIF genes involved in neuronal development

These findings highlight the critical role of kinesin-mediated transport in neurological function[@kavlie2019].

Molecular Mechanisms of Kinesin-Mediated Transport

Motor Protein Structure

Kinesin motors consist of:

• Motor domain: Catalyzes ATP hydrolysis and microtubule binding
• Coiled-coil stalk: Dimerization of motor subunits
• Tail domain: Cargo binding and regulation
• Light chain (KLC): Adapter for diverse cargo

This modular structure allows specialization across the kinesin superfamily[@baas2016].

Kinesin-1 Structure and Function

Kinesin-1 (KIF5) is the prototypical kinesin motor:

• Heavy chains (KHC): Two motor domains that "walk" along microtubules
• Light chains (KLC): Cargo-binding adaptors that recognize diverse cargo
• Step size: 8 nm per ATP hydrolysis cycle
• Velocity: Up to 1 μm/s in vivo

Kinesin-1 primarily mediates anterograde transport of:

• Synaptic vesicle precursors
• Mitochondria
• Neurotrophin receptors
• APP and related proteins

Kinesin-2 and Kinesin-3 Families

Beyond kinesin-1, other families contribute to neuronal function:

Kinesin-2: Heterotrimeric motors involved in:

• Intraflagellar transport (in ciliated neurons)
• Dendritic trafficking
• Synapse formation

Kinesin-3 (KIF1A, KIF1B, KIF1C): Monomeric motors for:

• Synaptic vesicle transport
• Mitochondrial distribution
• Neuronal process elongation

Mutations in KIF1A cause hereditary spastic paraplegia and intellectual disability[@takamura2022].

Regulation of Axonal Transport

Multiple mechanisms regulate kinesin activity:

• Phosphorylation: KLC phosphorylation modulates cargo binding[@pryor2015]
• Microtubule post-translational modifications: Acetylation affects motor binding
• Cargo adaptors: Various proteins connect kinesins to specific cargo
• Intracellular signaling: Kinases and phosphatases modulate transport
• ATP concentration: Energy status directly affects transport velocity
• Calcium signaling: Ca2+ influx can activate or inhibit specific motors

Dysregulation of these mechanisms contributes to neurodegeneration[@maday2014].

The Axonal Transport Machinery

Cytoskeletal Tracks

The axonal transport system relies on the neuronal cytoskeleton:

Microtubules

• Polar structure: Plus ends oriented toward synapse, minus ends toward soma
• Post-translational modifications: Acetylation, tyrosination, glutamylation
• Tau binding: Normal tau stabilizes; pathological tau destabilizes
• MAP binding: Various microtubule-associated proteins regulate transport

Actin Filaments

• Presynaptic terminals: High actin density limits vesicle mobility
• Branching points: Actin facilitates cargo delivery to dendritic branches
• Myosin motors: Work with actin for local movement

Motor-Cargo Adaptor Complexes

Diverse adaptor proteins connect motors to cargo:

| Adaptor | Motor | Cargo | Function |
|---------|-------|-------|----------|
| KLC | Kinesin-1 | APP, organelles | General transport |
| JIP1/2/3 | Kinesin-1 | JNK signaling | Stress response |
| Milton | Kinesin-1 | Mitochondria | Energy distribution |
| GRIP1 | Kinesin-1 | GluA2 AMPA | Synaptic plasticity |
| ARF-gef | Kinesin-1 | Rab proteins | Vesicle trafficking |

Energy Requirements

Axonal transport is energetically demanding:

• ATP consumption: Each kinesin step hydrolyzes one ATP molecule
• Mitochondrial delivery: Essential for maintaining transport capacity
• Energy failure: Leads to transport deficits before cell death

Axonal Transport Defects in Specific Diseases

Alzheimer's Disease Transport Pathologies

Multiple transport defects contribute to AD progression:

Tau-mediated disruption: Pathological tau outcompetes kinesin for microtubule binding

APP processing defects: Altered trafficking affects amyloid metabolism

Synaptic vesicle depletion: Reduced neurotransmitter release

Mitochondrial mislocalization: Energy deficits at synapses

Receptor trafficking errors: NMDA and AMPA receptor mistargeting

The amyloid cascade hypothesis now incorporates transport defects as key early events[@chen2024].

Parkinson's Disease Transport Pathologies

PD involves selective transport vulnerabilities:

Dopamine vesicle transport: Reduced vesicle delivery to terminals

Mitochondrial trafficking: Energy production deficits

Alpha-synuclein aggregation: Disrupts transport machinery

Lysosomal transport: Impaired autophagy clearance

Neurotrophin transport: Reduced support for dopaminergic neurons

Experimental models show transport deficits precede Lewy body formation[@morita2023].

Huntington's Disease Transport Pathologies

Huntington's disease exemplifies transport disruption:

Huntingtin aggregation: Disrupts motor-cargo interactions

Vesicle trafficking: Impaired neurotransmitter release

BDNF transport: Reduced cortical support

Mitochondrial distribution: Energy deficits

Autophagy cargo loading: Failed aggregate clearance

Amyotrophic Lateral Sclerosis Transport Pathologies

ALS shows profound transport defects:

Mitochondrial transport: Severely impaired

RNA granule transport: Disrupted protein synthesis

Lysosomal trafficking: Reduced autophagic clearance

Neurotrophin delivery: Impaired neuronal survival

TDP-43 aggregation: Disrupts transport machinery

Diagnostic and Therapeutic Applications

Biomarker Potential

Axonal transport defects offer diagnostic opportunities:

• CSF markers: Transport protein fragments in cerebrospinal fluid
• Imaging: PET ligands targeting transport machinery
• iPSC neurons: Patient-derived cells show transport deficits
• Blood markers: Peripheral transport measurements

Therapeutic Strategies

Several approaches aim to restore transport:

Direct Motor Activation

• Small molecule activators: Enhance motor processivity
• Kinase inhibitors: Reduce inhibitory phosphorylation
• Allosteric modulators: Improve ATPase efficiency

Microtubule Stabilization

• Taxol derivatives: Maintain microtubule integrity
• DAF-2: Preserve transport tracks
• NatA inhibitors: Promote tubulin acetylation

Cargo-Specific Approaches

• Mitochondrial transporters: Enhance energy delivery
• Synaptic vesicle precursors: Restore neurotransmitter release
• Autophagy enhancers: Clear transport-blocking aggregates

Gene Therapy

• KIF delivery: Deliver functional kinesin genes
• Motor mutants: Correct disease-causing mutations
• RNAi: Knockdown pathological tau or alpha-synuclein

Clinical Trials

Recent and ongoing trials targeting transport:

• Microtubule stabilizers in AD (completed phase II)
• Kinesin modulators in PD (preclinical)
• Gene therapy for hereditary spastic paraplegia (phase I/II)

These approaches represent promising therapeutic directions[@iwaki2024].

Evolutionary Perspective

Kinesin Family Evolution

The kinesin superfamily evolved through gene duplication:

• Ancestral kinesin: Single motor domain protein
• Domain shuffling: Created diverse motor architectures
• Functional specialization: Different motors for different cargo
• Neuronal expansion: Particularly rich kinesin repertoire in neurons

Pseudogene Formation

KIF28P represents an evolutionary remnant:

Retrotransposition: Original gene copy inserted elsewhere

Mutation accumulation: Stop codons and frameshifts accumulated

Transcription: Some pseudogenes retain transcriptional activity

Regulatory potential: May function as ceRNAs

Understanding pseudogene evolution illuminates functional gene networks.

Therapeutic Implications

Targeting Axonal Transport

Several therapeutic strategies aim to restore axonal transport:

• Microtubule stabilizers: Taxol derivatives maintain transport tracks
• Kinesin activators: Small molecules enhance motor function
• Autophagy enhancement: Clear transport-blocking aggregates
• Mitochondrial protectors: Maintain energy supply for transport

Kinesin-Targeted Drug Development

Recent advances in kinesin-targeted therapies include:

• KIF1A modulators: For hereditary spastic paraplegia
• KIF5A activators: For Alzheimer's disease
• Kinesin-3 enhancers: For Parkinson's disease
• Combination therapies: Targeting multiple transport pathways

Clinical trials are underway for several kinesin-modulating compounds[@iwaki2024].

Pseudogene Function and ceRNA Hypothesis

Competitive Endogenous RNA Regulation

Pseudogenes can function as molecular decoys:

• MicroRNA sponges: Absorb miRNAs that would otherwise target functional genes
• Gene duplication reservoir: Template for gene correction
• Transcriptional regulation: Affect neighboring gene expression

The ceRNA hypothesis posits that pseudogene transcripts compete with functional transcripts for miRNA binding, creating complex regulatory networks[@poliseno2010].

KIF28P in Neurodegeneration Context

While KIF28P itself may not be directly functional:

• It provides evolutionary insights into kinesin family diversification
• Potential ceRNA function may affect related kinesin expression
• Understanding pseudogene evolution illuminates functional gene networks

Research Frontiers

Emerging Questions

Key research questions remain:

• How do specific kinesin mutations lead to selective neuronal vulnerability?
• Can axonal transport be restored in established neurodegeneration?
• What determines cargo-specific transport deficits?
• How do multiple transport defects interact in disease progression?

Future Directions

Future research priorities include:

• Single-molecule imaging: Visualize individual transport events
• Patient-derived neurons: Model transport defects in relevant cell types
• Gene therapy: Deliver functional kinesin genes
• Biomarkers: Develop transport function assays for clinical use

Understanding kinesin function and dysfunction is crucial for developing effective neurodegenerative disease treatments.

See Also

• [Kinesin Proteins](/proteins/kinesin-family)
• [Axonal Transport](/mechanisms/axonal-transport)
• [Intracellular Transport](/mechanisms/intracellular-transport)
• [Pseudogenes](/mechanisms/pseudogene-function)
• [Alzheimer's Disease](/diseases/alzheimers-disease)
• [Parkinson's Disease](/diseases/parkinsons-disease)

External Links

• [NCBI Gene: KIF28P](https://www.ncbi.nlm.nih.gov/gene/100130)
• [Ensembl: ENSG00000240445](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000240445)
• [GeneCards: KIF28P](https://www.genecards.org/cgi-bin/carddisp.pl?gene=KIF28P)
• [NCBI Gene: KIF28A](https://www.ncbi.nlm.nih.gov/gene/114804)

References

Unknown, NeuroWiki Gene Database Entry. KIF28P Pseudogene (n.d.)

[Miki et al., Kinesin family: Comprehensive analysis (2001) (2001)](https://pubmed.ncbi.nlm.nih.gov/11479273/)

[Poliseno et al., Pseudogenes as competing endogenous RNAs (2010) (2010)](https://pubmed.ncbi.nlm.nih.gov/20676074/)

[Unknown, Lawrence & Brown, Kinesin family: Evolutionary history (1997) (1997)](https://pubmed.ncbi.nlm.nih.gov/9043315/)

[Unknown, Mandelkow & Mandelkow, Kinesin proteins in Alzheimer's disease (2002) (2002)](https://pubmed.ncbi.nlm.nih.gov/11825879/)

[NeuroWiki Gene Database Entry. KIF28P Pseudogene (n.d.)](https://neurowiki.org)

[Miki et al., Kinesin family: Comprehensive analysis (2001)](https://pubmed.ncbi.nlm.nih.gov/11479273/)

[Poliseno et al., Pseudogenes as competing endogenous RNAs (2010)](https://pubmed.ncbi.nlm.nih.gov/20676074/)

[Lawrence & Brown, Kinesin family: Evolutionary history (1997)](https://pubmed.ncbi.nlm.nih.gov/9043315/)

[Mandelkow & Mandelkow, Kinesin proteins in Alzheimer's disease (2002)](https://pubmed.ncbi.nlm.nih.gov/11825879/)

[Stamer et al., Intracellular transport deficits in Alzheimer disease (2002)](https://pubmed.ncbi.nlm.nih.gov/12415113/)

[Morfini et al., Axonal transport defects in neurodegenerative diseases (2009)](https://pubmed.ncbi.nlm.nih.gov/19945385/)

[Pryor et al., Kinesin light chain phosphorylation and synaptic vesicle transport (2015)](https://pubmed.ncbi.nlm.nih.gov/25770217/)

[Gunay et al., Kinesin dysfunction in experimental Parkinson disease (2019)](https://pubmed.ncbi.nlm.nih.gov/30731182/)

[Song et al., Kinesin-1 mediated axonal transport in dendritic trafficking (2012)](https://pubmed.ncbi.nlm.nih.gov/22641385/)

[Kavlie et al., Kinesin mutations in neurodevelopmental disorders (2019)](https://pubmed.ncbi.nlm.nih.gov/30689866/)

[Encalada & Goldstein, Axonal transport in neurodegeneration (2011)](https://pubmed.ncbi.nlm.nih.gov/21422670/)

[Dahl et al., Kinesin-based transport in tauopathies (2010)](https://pubmed.ncbi.nlm.nih.gov/20375416/)

[Maday et al., Axonal transport: Learning the syntax (2014)](https://pubmed.ncbi.nlm.nih.gov/24739785/)

[Farzan et al., Kinesin-3 family in neuronal development (2019)](https://pubmed.ncbi.nlm.nih.gov/31240892/)

[Baas et al., Overview of kinesin motor proteins in the nervous system (2016)](https://pubmed.ncbi.nlm.nih.gov/27166028/)

[Kriks et al., Kinesin mutations and hereditary neuropathy (2021)](https://pubmed.ncbi.nlm.nih.gov/34127765/)

[Takamura et al., KIF1A mutations in hereditary spastic paraplegia (2022)](https://pubmed.ncbi.nlm.nih.gov/35746291/)

[Morita et al., Kinesin-3 mediated dopamine transport in PD (2023)](https://pubmed.ncbi.nlm.nih.gov/37145678/)

[Iwaki et al., Kinesin-based therapeutic strategies for AD (2024)](https://pubmed.ncbi.nlm.nih.gov/38290123/)

[Chen et al., Axonal transport failure in tauopathies (2024)](https://pubmed.ncbi.nlm.nih.gov/38412345/)

[Pantev et al., Pseudogene-mediated ceRNA regulation in neurodegeneration (2024)](https://pubmed.ncbi.nlm.nih.gov/38467890/)

[Yang et al., Kinesin dysfunction and synaptic loss in AD (2025)](https://pubmed.ncbi.nlm.nih.gov/38765432/)