Tau-Independent Microtubule Stabilization via MAP6 Enhancement
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From Analysis:
Selective vulnerability of entorhinal cortex layer II neurons in AD
Why do entorhinal cortex layer II stellate neurons die first in AD? Their unique electrophysiological properties, grid cell function, and high metabolic demand may contribute, but the molecular basis of selective vulnerability is unknown.
Hypotheses from Same Analysis (6)
These hypotheses emerged from the same multi-agent debate that produced this hypothesis.
Description
Mechanistic Overview
Tau-Independent Microtubule Stabilization via MAP6 Enhancement starts from the claim that modulating MAP6 within the disease context of neurodegeneration can redirect a disease-relevant process. The original description reads: "Tau-independent microtubule stabilization via MAP6 (also known as STOP protein — Stable Tubule Only Polypeptide) enhancement proposes compensating for tau loss-of-function by upregulating an alternative microtubule-stabilizing protein....
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Curated Mechanism Pathway
Curated pathway diagram from expert analysis
flowchart TD
A["Microtubule Lattice"]
B["Tau Protein"]
C["MAP6/STOP Protein"]
D["GSK3beta/CDK5 Kinases"]
E["Tau Hyperphosphorylation"]
F["Tau Detachment from MT"]
G["Tau Aggregation NFTs"]
H["MAP6 Decline"]
I["NF-kappaB Repression"]
J["Calpain Degradation"]
K["miR-132 Loss"]
L["Cytoskeletal Collapse"]
M["HDAC Inhibitors"]
N["miR-132 Mimics"]
O["Calpain Inhibitors"]
P["MAP6 Enhancement"]
Q["MT Stabilization Recovery"]
A --> B
A --> C
B -->|"Normal binding"| A
C -->|"Cold-stable binding"| A
D -->|"Hyperactivation"| E
E --> F
E --> G
F -->|"Loss of function"| L
G -->|"Pathological"| L
I -->|"Transcriptional repression"| H
J -->|"Protein degradation"| H
K -->|"mRNA destabilization"| H
H -->|"Contributes to"| L
M -->|"Increases transcription"| P
N -->|"Stabilizes mRNA"| P
O -->|"Prevents degradation"| P
P -->|"Compensates for tau loss"| Q
Q --> A
classDef normal fill:#4fc3f7
classDef pathological fill:#ef5350
classDef therapeutic fill:#81c784
classDef regulatory fill:#ce93d8
class A,B,C normal
class D,E,F,G,H,I,J,K,L pathological
class M,N,O,P,Q therapeutic
3D Protein Structure (AlphaFold)
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✓ Supporting Evidence 14
Corticostriatal projections originate from the entire cerebral cortex and provide the major source of glutamatergic inputs to the basal ganglia. Despite the importance of corticostriatal connections in sensorimotor learning and cognitive functions, plasticity forms at these synapses remain strongly debated. Using a corticostriatal slice preserving the connections between the somatosensory cortex and the target striatal cells, we report the induction of both non-Hebbian and Hebbian forms of long-term potentiation (LTP) and long-term depression (LTD) on striatal output neurons (SONs). LTP and LTD can be induced selectively by different stimulation patterns (high-frequency trains vs low-frequency pulses) and were evoked with similar efficiency in non-Hebbian and Hebbian modes. Combination of LTP-LTD and LTD-LTP sequences revealed that bidirectional plasticity occurs at the same SONs and provides efficient homeostatic mechanisms leading to a resetting of corticostriatal synapses avoiding s
Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], a seleno-organic compound with glutathione peroxidase-like activity is used in clinical trials against stroke. Human and bovine TrxR catalyzed the reduction of ebselen to ebselen selenol by NADPH with an apparent K(M)-value of 2.5 microM and a kcat of 588 min(-1). The addition of thioredoxin (Trx) stimulated the TrxR-catalyzed reduction of ebselen several-fold. This result was caused by a very fast oxidation of reduced Trx by ebselen with a rate constant in excess of 2 x 10(7) M(-1) s(-1). This rate is orders of magnitude faster than the reaction of dithiol Trx with insulin disulfides. Ebselen competed with disulfide substrates for reduction by Trx and, therefore, acted as an inhibitor of protein disulfide reduction by the Trx system. The inherent H2O2 reductase activity of mammalian TrxR dependent on its active-site selenocysteine residue was stimulated 10-fold by 2 microM ebselen and 25-fold in the additional presence of 5 microM Trx
Observable patterns of cultural variation are consistently intertwined with demic movements, cultural diffusion, and adaptation to different ecological contexts [Cavalli-Sforza and Feldman (1981) Cultural Transmission and Evolution: A Quantitative Approach; Boyd and Richerson (1985) Culture and the Evolutionary Process]. The quantitative study of gene-culture coevolution has focused in particular on the mechanisms responsible for change in frequency and attributes of cultural traits, the spread of cultural information through demic and cultural diffusion, and detecting relationships between genetic and cultural lineages. Here, we make use of worldwide whole-genome sequences [Pagani et al. (2016) Nature 538:238-242] to assess the impact of processes involving population movement and replacement on cultural diversity, focusing on the variability observed in folktale traditions (n = 596) [Uther (2004) The Types of International Folktales: A Classification and Bibliography. Based on the Sy
Major depression affects multiple physiologic systems. Therefore, analysis of signals that reflect integrated function may be useful in probing dynamical changes in this syndrome. Increasing evidence supports the conceptual framework that complex variability is a marker of healthy, adaptive control mechanisms and that dynamical complexity decreases with aging and disease. We tested the hypothesis that heart rate (HR) dynamics in non-medicated, young to middle-aged males during an acute major depressive episode would exhibit lower complexity compared with healthy counterparts. We analyzed HR time series, a neuroautonomically regulated signal, during sleep, using the multiscale entropy method. Our results show that the complexity of the HR dynamics is significantly lower for depressed than for non-depressed subjects for the entire night (P<0.02) and combined sleep stages 1 and 2 (P<0.02). These findings raise the possibility of using the complexity of physiologic signals as the basis of
The functional and molecular similarities and distinctions between human and murine astrocytes are poorly understood. Here, we report the development of an immunopanning method to acutely purify astrocytes from fetal, juvenile, and adult human brains and to maintain these cells in serum-free cultures. We found that human astrocytes have abilities similar to those of murine astrocytes in promoting neuronal survival, inducing functional synapse formation, and engulfing synaptosomes. In contrast to existing observations in mice, we found that mature human astrocytes respond robustly to glutamate. Next, we performed RNA sequencing of healthy human astrocytes along with astrocytes from epileptic and tumor foci and compared these to human neurons, oligodendrocytes, microglia, and endothelial cells (available at http://www.brainrnaseq.org). With these profiles, we identified novel human-specific astrocyte genes and discovered a transcriptome-wide transformation between astrocyte precursor cel
Tau loss of function from microtubules contributes to axonal transport failure independently of aggregation to… MEDIUM▼
Mislocalization and aggregation of Aβ and Tau combined with loss of synapses and microtubules (MTs) are hallmarks of Alzheimer disease. We exposed mature primary neurons to Aβ oligomers and analysed changes in the Tau/MT system. MT breakdown occurs in dendrites invaded by Tau (Tau missorting) and is mediated by spastin, an MT-severing enzyme. Spastin is recruited by MT polyglutamylation, induced by Tau missorting triggered translocalization of TTLL6 (Tubulin-Tyrosine-Ligase-Like-6) into dendrites. Consequences are spine loss and mitochondria and neurofilament mislocalization. Missorted Tau is not axonally derived, as shown by axonal retention of photoconvertible Dendra2-Tau, but newly synthesized. Recovery from Aβ insult occurs after Aβ oligomers lose their toxicity and requires the kinase MARK (Microtubule-Affinity-Regulating-Kinase). In neurons derived from Tau-knockout mice, MTs and synapses are resistant to Aβ toxicity because TTLL6 mislocalization and MT polyglutamylation are prev
The development and function of the central nervous system rely on the microtubule (MT) and actin cytoskeletons and their respective effectors. Although the structural role of the cytoskeleton has long been acknowledged in neuronal morphology and activity, it was recently recognized to play the role of a signaling platform. Following this recognition, research into Microtubule Associated Proteins (MAPs) diversified. Indeed, historically, structural MAPs-including MAP1B, MAP2, Tau, and MAP6 (also known as STOP);-were identified and described as MT-binding and -stabilizing proteins. Extensive data obtained over the last 20 years indicated that these structural MAPs could also contribute to a variety of other molecular roles. Among multi-role MAPs, MAP6 provides a striking example illustrating the diverse molecular and cellular properties of MAPs and showing how their functional versatility contributes to the central nervous system. In this review, in addition to MAP6's effect on microtub
We previously documented that individual microtubules in the axons of cultured juvenile rodent neurons consist of a labile domain and a stable domain and that experimental depletion of tau results in selective shortening and partial stabilization of the labile domain. After first confirming these findings in adult axons, we sought to understand the mechanism that accounts for the formation and maintenance of these microtubule domains. We found that fluorescent tau and MAP6 ectopically expressed in RFL-6 fibroblasts predominantly segregate on different microtubules or different domains on the same microtubule, with the tau-rich ones becoming more labile than in control cells and the MAP6-rich ones being more stable than in control cells. These and other experimental findings, which we studied further using computational modeling with tunable parameters, indicate that these two MAPs do not merely bind to pre-existing stable and labile domains but actually create stable and labile domains
Association of tau (encoded by Mapt) with microtubules causes them to be labile, whereas association of MAP6 with microtubules causes them to be stable. As axons differentiate and grow, tau and MAP6 segregate from one another on individual microtubules, resulting in the formation of stable and labile domains. The functional significance of the yin-yang relationship between tau and MAP6 remains speculative, with one idea being that such a relationship assists in balancing morphological stability with plasticity. Here, using primary rodent neuronal cultures, we show that tau depletion has opposite effects compared to MAP6 depletion on the rate of neuronal development, the efficiency of growth cone turning, and the number of neuronal processes and axonal branches. Opposite effects to those seen with tau depletion were also observed on the rate of neuronal migration, in an in vivo assay, when MAP6 was depleted. When tau and MAP6 were depleted together from neuronal cultures, the morphologi
Microtubules assembled from purified tubulin in vitro are labile, rapidly disassembling when exposed to a variety of depolymerizing conditions such as cold temperature. In contrast, in many cell types, microtubules seem to be unaffected when the cell is exposed to the cold. This resistance of microtubules to the cold has been intriguing because the earliest and by far most studied microtubule-associated proteins such as MAP2 and tau are devoid of microtubule cold stabilizing activity. Over the past several years, it has been shown that resistance of microtubules to the cold is largely due to polymer association with a class of microtubule-associated proteins called STOPs. STOPs are calmodulin-binding and calmodulin-regulated proteins which, in mammals, are encoded by a single gene but exhibit substantial cell specific variability due to mRNA splicing and alternative promoter use. STOP microtubule stabilizing activity has been ascribed to two classes of new bifunctional calmodulin- and
Microtubules assembled from pure tubulin in vitro are labile, rapidly depolymerized upon exposure to the cold. In contrast, in a number of cell types, cytoplasmic microtubules are stable, resistant to prolonged cold exposure. During the past years, the molecular basis of this microtubule stabilization in cells has been elucidated. Cold stability is due to polymer association with different variants of a calmodulin-regulated protein, STOP protein. The dynamic and hence the physiological consequences of STOP association with microtubules vary in different tissues. In neurons, STOP seems almost permanently associated with microtubules. STOP is apparently a major determinant of microtubule turnover in such cells and is required for normal neuronal differentiation. In cycling cells, only minor amounts of STOP are associated with interphase microtubules and STOP does not measurably affects microtubule dynamics. However, STOP is associated with mitotic microtubules in the spindle. Recent resu
Microtubule-associated Protein 6 (MAP6) is critical for maintaining microtubule stability and synaptic plasticity, and its dysfunction is a key driver of cognitive impairment. However, the molecular mechanisms linking MAP6 deletion to cognitive deficits remain unclear. Here, we generated a novel Map6 knockout (KO, Map6-/-) mouse model using CRISPR/Cas9-mediated genome editing. Behavioral tests confirmed that Map6-/- mice exhibited prominent cognitive impairments, primarily in long-term memory and spatial learning. Hippocampal transcriptome profiling identified marked downregulation of neurotensin (Nts) in Map6-/- mice, which was validated at both mRNA and protein levels. Rescue experiments demonstrated that direct microinjection of neurotensin (NTS) peptide into the hippocampal CA1 subregion significantly improved cognitive deficits in Map6-/- mice. Electrophysiological recordings further confirmed that NTS restored impaired long-term potentiation (LTP)-a cellular substrate of learning
Targeting CXCL16-expressing macrophages with a biomimetic nanocarrier system attenuates cartilage degeneration… MEDIUM▼
Osteoarthritis (OA) is a whole-joint disorder characterized by progressive cartilage degradation and chronic synovial inflammation, in which macrophages play a central role. Using single-cell RNA sequencing of human and mouse synovial tissues, we identified a pronounced expansion of macrophages during OA progression, with nearly ubiquitous expression of the chemokine CXCL16. These CXCL16+ macrophages exhibited a pro-inflammatory phenotype and were strongly associated with synovitis. To exploit this target, we developed a biomimetic nanoparticle (MAP6) by coating capsaicin-loaded poly(lactic-co-glycolic acid) (PLGA) with CXCR6-enriched M1 macrophage membranes, leveraging the specific CXCL16-CXCR6 interaction. The resulting MAP6 nanoparticles demonstrated enhanced cellular uptake, prolonged synovial retention, and specific targeting of CXCL16+ macrophages in vivo. Furthermore, MAP6 treatment promoted Ca2+ influx and NRF2 nuclear translocation, thereby suppressing pro-inflammatory cytokin
BioID2-Based Tau Interactome Reveals Novel and Known Protein Interactions Associated with Multiple Cellular Pa… MEDIUM▼
Pathological inclusions composed of tau are hallmarks of neurodegenerative diseases termed tauopathies, the most common of which is Alzheimer's disease. Accumulating evidence suggests that tau is involved in a multitude of physiological functions that are regulated, in part, by direct and/or transient protein interactions. Deciphering the tau interactome is critical for understanding the physiological and pathological roles of tau. This work aimed to identify potential tau interactors using the in situ protein labeling biotin identification (BioID2) method. Advantages of this approach include in-cell interactor labeling and an enhanced likelihood of detecting transient and/or weak interactions. We identified 324 potential tau interactors spanning multiple cellular compartments and pathways. We validated tau interactions with selected candidates using two independent approaches: proximity ligation assay and co-immunoprecipitation (co-IP) which included cytoskeletal proteins (MAP2 and MA
✗ Opposing Evidence 5
Tau is a multifunctional microtubule-associated protein in the neuron. For decades, tau's main function in neurons has been broadly accepted as stabilizing microtubules in the axon; however, this conclusion was reached mainly on the basis of studies performed in vitro and on ectopic expression of tau in non-neuronal cells. The idea has become so prevailing that some disease researchers are even seeking to use microtubule-stabilizing drugs to treat diseases in which tau dissociates from microtubules. Recent work suggests that tau is not a stabilizer of microtubules in the axon, but rather enables axonal microtubules to have long labile domains, in part by outcompeting genuine stabilizers. This new perspective on tau challenges long-standing dogma.
Neurons are terminally differentiated cells that use their microtubule arrays not for cell division but rather as architectural elements required for the elaboration of elongated axons and dendrites. In addition to acting as compression-bearing struts that provide for the shape of the neuron, microtubules also act as directional railways for organelle transport. The stability properties of neuronal microtubules are commonly discussed in the biomedical literature as crucial to the development and maintenance of the nervous system, and have recently gained attention as central to the etiology of neurodegenerative diseases. Drugs that affect microtubule stability are currently under investigation as potential therapies for disease and injury of the nervous system. There is often a lack of consistency, however, in how the issue of microtubule stability is discussed in the literature, and this can affect the design and interpretation of experiments as well as potential therapeutic regimens.
Recent advancements in gene expression modulation and RNA delivery systems have underscored the immense potential of nucleic acid-based therapies (NA-BTs) in biological research. However, the blood-brain barrier (BBB), a crucial regulatory structure that safeguards brain function, presents a significant obstacle to the delivery of drugs to glial cells and neurons. The BBB tightly regulates the movement of substances from the bloodstream into the brain, permitting only small molecules to pass through. This selective permeability poses a significant challenge for effective therapeutic delivery, especially in the case of NA-BTs. Extracellular vesicles, particularly exosomes, are recognized as valuable reservoirs of potential biomarkers and therapeutic targets. They are also gaining significant attention as innovative drug and nucleic acid delivery (NAD) carriers. Their unique ability to safeguard and transport genetic material, inherent biocompatibility, and capacity to traverse physiolog
ReMAPping the microtubule landscape: How phosphorylation dictates the activities of microtubule-associated pro… MEDIUM▼
Classical microtubule-associated proteins (MAPs) were originally identified based on their co-purification with microtubules assembled from mammalian brain lysate. They have since been found to perform a range of functions involved in regulating the dynamics of the microtubule cytoskeleton. Most of these MAPs play integral roles in microtubule organization during neuronal development, microtubule remodeling during neuronal activity, and microtubule stabilization during neuronal maintenance. As a result, mutations in MAPs contribute to neurodevelopmental disorders, psychiatric conditions, and neurodegenerative diseases. MAPs are post-translationally regulated by phosphorylation depending on developmental time point and cellular context. Phosphorylation can affect the microtubule affinity, cellular localization, or overall function of a particular MAP and can thus have profound implications for neuronal health. Here we review MAP1, MAP2, MAP4, MAP6, MAP7, MAP9, tau, and DCX, and how each
This review focuses on the discovery of activity-dependent neuroprotective protein (ADNP) and the ensuing discovery of NAP (davunetide) toward clinical development with emphasis on microtubule protection. ADNP immunoreactivity was shown to occasionally decorate microtubules and ADNP silencing inhibited neurite outgrowth as measured by microtubule associated protein 2 (MAP2) labeling. ADNP knockout is lethal, while 50% reduction in ADNP (ADNP haploinsufficiency) resulted in the microtubule associated protein tau pathology coupled to cognitive dysfunction and neurodegeneration. NAP (davunetide), an eight amino acid peptide derived from ADNP partly ameliorated deficits associated with ADNP deficiency. NAP (davunetide) interacted with microtubules, protected against microtubule toxicity associated with zinc, nocodazole and oxidative stress in vitro and against tau pathology and MAP6 (stable tubuleonly polypeptide - STOP) pathology in vivo. NAP (davunetide) provided neurotrophic functions p
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses ▼
Novel Therapeutic Hypotheses for Entorhinal Cortex Layer II Selective Vulnerability in AD
1. HCN1-Mediated Resonance Frequency Stabilization Therapy
Description: EC layer II stellate neurons exhibit unique 4-8 Hz membrane resonance frequencies critical for grid cell oscillations, mediated by HCN1 channels. Therapeutic enhancement of HCN1 channel function could maintain proper membrane resonance and prevent the metabolic cascade leading to neuronal death by preserving efficient theta-gamma coupling.Target: HCN1 (hyperpolarization-activated cyclic nucleotide-gated channel 1)
**S
🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns ▼
Critical Evaluation of EC Layer II Therapeutic Hypotheses
1. HCN1-Mediated Resonance Frequency Stabilization Therapy
Specific Weaknesses:
- The hypothesis assumes HCN1 dysfunction is causal rather than consequential to AD pathology. HCN1 downregulation could be a protective response to excessive excitation
- Grid cell dysfunction may result from upstream circuit-level changes, not intrinsic membrane properties
- No evidence that restoring resonance frequencies in diseased neurons would be beneficial rather than harmful
- HCN1 enhancement increases neuronal exc
🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation ▼
Druggability Assessment of EC Layer II Therapeutic Hypotheses
HYPOTHESIS 3: Reelin-Mediated Cytoskeletal Stabilization (Revised Confidence: 0.55)
Druggability Assessment: MODERATE-LOW
Target: RELN pathway (Reelin, DAB1, LIS1)Chemical Matter Challenges:
- Reelin is a large extracellular matrix protein (3461 amino acids) - not directly druggable with small molecules
- Must target downstream signaling (ApoER2/VLDLR receptors, DAB1 phosphorylation)
- Blood-brain barrier penetration required for central targets
- None in clinical development for
⚖ Synthesizer Integrates perspectives and produces final ranked assessments ▼
Price History
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| 📄 | New Evidence | $0.508 | ▲ 1.7% | evidence_batch_update | 2026-04-13 02:18 |
| 📄 | New Evidence | $0.500 | ▲ 4.0% | evidence_batch_update | 2026-04-13 02:18 |
| ⚖ | Recalibrated | $0.480 | ▼ 0.4% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.482 | ▼ 1.3% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.488 | ▲ 1.5% | 2026-04-10 14:28 | |
| ⚖ | Recalibrated | $0.481 | ▲ 2.2% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.471 | ▲ 1.0% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.466 | ▼ 0.7% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.469 | ▼ 2.2% | 2026-04-04 16:02 | |
| 📄 | New Evidence | $0.480 | ▲ 2.6% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.468 | ▼ 21.3% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.595 | ▲ 7.9% | market_dynamics | 2026-04-03 01:06 |
| ⚖ | Recalibrated | $0.551 | ▲ 11.6% | market_dynamics | 2026-04-03 01:06 |
| ⚖ | Recalibrated | $0.494 | ▲ 3.2% | 2026-04-02 21:55 | |
| ⚖ | Recalibrated | $0.479 | ▼ 4.4% | market_recalibrate | 2026-04-02 19:14 |
Clinical Trials (6) Relevance: 5%
Active
Completed
Total Enrolled
Highest Phase
📚 Cited Papers (38)
📙 Related Wiki Pages (15)
📓 Linked Notebooks (1)
📊 Resource Economics & ROI
Cost Ratios
Score Impact
How Economics Pricing Works
Hypotheses receive an efficiency score (0-1) based on how many knowledge graph edges and citations they produce per token of compute spent.
High-efficiency hypotheses (score >= 0.8) get a price premium in the market, pulling their price toward $0.580.
Low-efficiency hypotheses (score < 0.6) receive a discount, pulling their price toward $0.420.
Monthly batch adjustments update all composite scores with a 10% weight from efficiency, and price signals are logged to market history.
Efficiency Price Signals
| Date | Signal Price | Score |
|---|---|---|
| 2026-04-16T20:00 | $0.490 | 0.511 |
Wiki Pages
KG Entities (45)
Dependency Graph (0 upstream, 5 downstream)
Linked Experiments (10)
Related Hypotheses
Estimated Development
🧪 Falsifiable Predictions (1)
Knowledge Subgraph (115 edges)
activates (1)
associated with (5)
co associated with (21)
co discussed (41)
▸ Show 36 more
early vulnerability (1)
encodes (3)
implicated in (7)
▸ Show 2 more
mediates (1)
participates in (7)
phosphorylates (1)
prevents (1)
regulates (15)
▸ Show 10 more
therapeutic target (7)
Mechanism Pathway for MAP6
Molecular pathway showing key causal relationships underlying this hypothesis
graph TD
MAP6["MAP6"] -->|regulates| microtubule_stabilization["microtubule_stabilization"]
MAP6_1["MAP6"] -->|regulates| Tau_Independent_Microtubu["Tau-Independent Microtubule Stabilization via MAP6"]
Tau_Independent_Microtubu_2["Tau-Independent Microtubule Stabilization via MAP6"] -->|therapeutic target| Alzheimer_s_Disease["Alzheimer's Disease"]
MAP6_3["MAP6"] -->|associated with| neurodegeneration["neurodegeneration"]
MAP6_4["MAP6"] -->|regulates| Tau_Propagation["Tau Propagation"]
MAP6_5["MAP6"] -->|participates in| Microtubule_dynamics_and_["Microtubule dynamics and stabilization"]
RELN["RELN"] -->|co discussed| MAP6_6["MAP6"]
MAP6_7["MAP6"] -->|co discussed| HCN1["HCN1"]
MAP6_8["MAP6"] -->|co discussed| MCU["MCU"]
MAP6_9["MAP6"] -->|co discussed| IDH2["IDH2"]
PPARGC1A["PPARGC1A"] -->|co discussed| MAP6_10["MAP6"]
SLC16A2["SLC16A2"] -->|co discussed| MAP6_11["MAP6"]
HCN1_12["HCN1"] -->|co discussed| MAP6_13["MAP6"]
MCU_14["MCU"] -->|co discussed| MAP6_15["MAP6"]
IDH2_16["IDH2"] -->|co discussed| MAP6_17["MAP6"]
style MAP6 fill:#ce93d8,stroke:#333,color:#000
style microtubule_stabilization fill:#81c784,stroke:#333,color:#000
style MAP6_1 fill:#ce93d8,stroke:#333,color:#000
style Tau_Independent_Microtubu fill:#4fc3f7,stroke:#333,color:#000
style Tau_Independent_Microtubu_2 fill:#4fc3f7,stroke:#333,color:#000
style Alzheimer_s_Disease fill:#ef5350,stroke:#333,color:#000
style MAP6_3 fill:#ce93d8,stroke:#333,color:#000
style neurodegeneration fill:#ef5350,stroke:#333,color:#000
style MAP6_4 fill:#ce93d8,stroke:#333,color:#000
style Tau_Propagation fill:#ffd54f,stroke:#333,color:#000
style MAP6_5 fill:#ce93d8,stroke:#333,color:#000
style Microtubule_dynamics_and_ fill:#81c784,stroke:#333,color:#000
style RELN fill:#ce93d8,stroke:#333,color:#000
style MAP6_6 fill:#ce93d8,stroke:#333,color:#000
style MAP6_7 fill:#ce93d8,stroke:#333,color:#000
style HCN1 fill:#ce93d8,stroke:#333,color:#000
style MAP6_8 fill:#ce93d8,stroke:#333,color:#000
style MCU fill:#ce93d8,stroke:#333,color:#000
style MAP6_9 fill:#ce93d8,stroke:#333,color:#000
style IDH2 fill:#ce93d8,stroke:#333,color:#000
style PPARGC1A fill:#ce93d8,stroke:#333,color:#000
style MAP6_10 fill:#ce93d8,stroke:#333,color:#000
style SLC16A2 fill:#ce93d8,stroke:#333,color:#000
style MAP6_11 fill:#ce93d8,stroke:#333,color:#000
style HCN1_12 fill:#ce93d8,stroke:#333,color:#000
style MAP6_13 fill:#ce93d8,stroke:#333,color:#000
style MCU_14 fill:#ce93d8,stroke:#333,color:#000
style MAP6_15 fill:#ce93d8,stroke:#333,color:#000
style IDH2_16 fill:#ce93d8,stroke:#333,color:#000
style MAP6_17 fill:#ce93d8,stroke:#333,color:#000
Predicted Protein Structure
🔮 MAP6 — AlphaFold Prediction Q96JE9 Click to expand 3D viewer
Source Analysis
Selective vulnerability of entorhinal cortex layer II neurons in AD
neurodegeneration | 2026-04-01 | completed
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