Hypotheses

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This index provides navigation for the Hypotheses section of NeuroWiki, covering research hypotheses about neurodegenerative disease mechanisms, disease progression models, and therapeutic approaches.

_Total: 79 pages_

Alzheimer's Disease Hypotheses

flowchart TD hypotheses["Hypotheses"] style hypotheses fill:#4fc3f7,stroke:#333,color:#000 hypotheses_0["Alzheimers Disease Hypotheses"] hypotheses -->|"includes"| hypotheses_0 style hypotheses_0 fill:#81c784,stroke:#333,color:#000 hypotheses_1["Disease Model and Progression"] hypotheses -->|"includes"| hypotheses_1 style hypotheses_1 fill:#ef5350,stroke:#333,color:#000 hypotheses_2["Tau and Propagation"] hypotheses -->|"includes"| hypotheses_2 style hypotheses_2 fill:#ffd54f,stroke:#333,color:#000 hypotheses_3["Cognitive and Network"] hypotheses -->|"includes"| hypotheses_3 style hypotheses_3 fill:#ce93d8,stroke:#333,color:#000 hypotheses_4["Mouse Model and Mechanistic"] hypotheses -->|"includes"| hypotheses_4 style hypotheses_4 fill:#4fc3f7,stroke:#333,color:#000 hypotheses_5["Parkinsons Disease Hypotheses"] hypotheses -->|"includes"| hypotheses_5 style hypotheses_5 fill:#81c784,stroke:#333,color:#000

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This index provides navigation for the Hypotheses section of NeuroWiki, covering research hypotheses about neurodegenerative disease mechanisms, disease progression models, and therapeutic approaches.

_Total: 79 pages_

Alzheimer's Disease Hypotheses

Mermaid diagram (expand to render)

[In Alzheimer's disease, biomarker events occur in a specific temporal sequence: amyloid-beta abnormalities precede tau abnormalities and neurodegeneration](/hypotheses/alzheimer's-disease,-biomarker-events-occur)
[Alzheimer's disease pathology originates in the hippocampus and subsequently spreads to other regions](/hypotheses/alzheimer's-disease-pathology-originates-hi)
[APOE contributes to Alzheimer's disease by regulating both beta-amyloid deposition and synaptic function](/hypotheses/apoe-contributes-alzheimer's-disease-regulat)
[Circadian-Glymphatic-Metabolic Coupling Failure Hypothesis in AD](/hypotheses/circadian-glymphatic-metabolic-coupling-alzheimers)
[Cellular Senescence Hypothesis in Alzheimer's Disease](/hypotheses/cellular-senescence-alzheimers)
[Neuritic Amyloid Plaques: Histomorphologic Evidence of Pathologic Synergy in AD](/hypotheses/hyp_37312)
[Pathologic synergy occurring in the amygdala between amyloid plaques and Tau/NFT may facilitate early cognitive decline](/hypotheses/pathologic-synergy-occurring-amygdala-betwe)

Disease Model and Progression

[Alzheimer's Disease Neuropathology is Defined by the Accumulation of Pathological Amyloid-Beta in the Form of Senile Plaques and Dystrophic Neurites, and Phosphorylated Tau Neurofibrillary Tangles](/hypotheses/hyp_15575)
[Amyloid plaque and neurofibrillary tangle deposition is an essential component for accurate modeling of AD in mouse models](/hypotheses/amyloid-plaque-neurofibrillary-tangle-depositi)
[Disease Model: Declining functional connectivity of the Default Mode Network in Alzheimer's Disease](/hypotheses/hyp_963428)
[Disease Model: In the absence of comorbid Ab, a-SN, or TDP-43 pathology, cognitive decline may be driven by other mechanisms](/hypotheses/hyp_367280)
[The Cortical/Transitional Zone of the Amygdala is Affected Early in Neurodegenerative Diseases](/hypotheses/hyp_146258)

Tau and Propagation

[Prion-Like Propagation of Proteinopathies: Template-Directed Misfolding in Neurodegeneration](/hypotheses/hyp_332160)
[Proteinopathic processes spread through the brain in a prion-like manner](/hypotheses/proteinopathic-processes-spread-through-brain)
[Prion vs Tau/Alpha-Synuclein Propagation: Mechanistic Comparison](/hypotheses/prion-vs-tau-alpha-syn-spread-comparison)
[Tau Pathology Severity Assessment Model: Braak Staging and Disease Progression](/hypotheses/hyp_436169)
[Amyloid-beta Plaques as Prerequisite for Isocortical Tau Spread in AD](/hypotheses/hyp_493636)

Cognitive and Network

[Bilateral Medial Temporal Lobe (MTL) Connectivity as Early Biomarker for Cognitive Decline](/hypotheses/hyp_382900)
[K-Cardinality Tree (KCT) Network Optimization for DMN Connectivity Analysis in Cognitive Decline](/hypotheses/hyp_409736)
[Alterations in Intra-Regional Functional Connectivity Within Default Mode Network Regions](/hypotheses/hyp_24486)
[Therapeutic Hypothesis: Both left and right medial temporal lobes (MTL) are affected early and may be rescued with targeted intervention](/hypotheses/hyp_493636)
[Therapeutic Hypothesis: TDP-43 and alpha-synuclein pathologies in the amygdala synergistically drive cognitive decline](/hypotheses/hyp_575716)

Mouse Model and Mechanistic

[Mechanistic Proposal: Chemical changes (namely hyperphosphorylation) occur in tau leading to NFT formation](/hypotheses/hyp_87091)
[Mechanistic Proposal: Amyloid Plaque and Neurofibrillary Tangle Deposition is Essential for Accurate Modeling of AD in Mouse Models](/hypotheses/hyp_871297)
[Mechanistic Proposal: Pathologic synergy between multiple proteinopathies drives disease progression](/hypotheses/hyp_885074)

Parkinson's Disease Hypotheses

Autophagy and Lysosomal Dysfunction

[Macroautophagy Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/macroautophagy-dysfunction-parkinsons)
[Chaperone-Mediated Autophagy Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/chaperone-mediated-autophagy-parkinsons)
[Mitochondria-Lysosome Contact Site (MLCS) Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/mlcs-dysfunction-parkinsons)
[Mitochondria-Lysosome Contact Site Dysfunction in Parkinson's Disease](/hypotheses/mitochondria-lysosome-contact-parkinsons)
[Mitochondria-Lysosome Contact Sites Dysfunction in Parkinson's Disease](/hypotheses/mlsm-axis-parkinsons)
[Retromer-Endosomal Sorting Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/retromer-endosomal-sorting-parkinsons)
[Lipid Droplet-Lysosome Axis Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/lipid-droplet-lysosome-axis-parkinsons)
[Proteasome-Ubiquitin System Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/proteasome-ubiquitin-system-dysfunction-parkinsons)
[TREM2-Alpha-Synuclein Clearance Hypothesis in Parkinson's Disease](/hypotheses/trem2-alpha-synuclein-clearance-parkinsons)

Mitochondrial and Metabolic

[DNA Damage Repair Deficiency Hypothesis in Parkinson's Disease](/hypotheses/dna-damage-repair-deficiency-parkinsons)
[Exercise-BDNF Signaling Axis Hypothesis in Parkinson's Disease](/hypotheses/exercise-bdnf-axis-parkinsons)
[Exercise-BDNF-Mitochondrial Resilience Hypothesis](/hypotheses/exercise-bdnf-mitochondrial-resilience-parkinsons)
[Metal Ion-Synuclein-Mitochondria Axis Hypothesis in Parkinson's Disease](/hypotheses/metal-ion-synuclein-mitochondria-axis-parkinsons)
[Mitochondrial Dynamics Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/mitochondrial-dynamics-dysfunction-parkinsons)
[Metabolic Syndrome-Parkinson's Disease Axis Hypothesis](/hypotheses/metabolic-syndrome-parkinsons-axis)
[Astrocyte-Neuron Metabolic Coupling Hypothesis in Parkinson's Disease](/hypotheses/astrocyte-neuron-metabolic-coupling-parkinsons)

Neuroinflammation

[cGAS-STING Pathway Dysregulation Hypothesis in Parkinson's Disease](/hypotheses/cgas-sting-parkinsons)
[NLRP3 Inflammasome Hypothesis in Parkinson's Disease](/hypotheses/nlrp3-inflammasome-parkinsons)
[Gut-Immune-Brain Axis Hypothesis in Parkinson's Disease](/hypotheses/gut-immune-brain-axis-parkinsons)
[Neurovascular Unit Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/neurovascular-unit-parkinsons)

Synuclein Propagation

[Extracellular Vesicle-Mediated Synuclein Propagation Hypothesis in Parkinson's Disease](/hypotheses/extracellular-vesicle-synuclein-propagation-parkinsons)
[Cellular Senescence Hypothesis in Parkinson's Disease](/hypotheses/cellular-senescence-parkinsons)
[Endocannabinoid System Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/endocannabinoid-system-dysfunction-parkinsons)
[Gap Junction Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/gap-junction-dysfunction-parkinsons)
[Ferroptosis Hypothesis in Parkinson's Disease](/hypotheses/ferroptosis-parkinsons)

Environmental and Systemic

[Environmental Toxin-Mitochondrial-Gut Axis Hypothesis in Parkinson's Disease](/hypotheses/environmental-toxin-mitochondrial-gut-axis-parkinsons)
[Viral Trigger Hypothesis in Parkinson's Disease](/hypotheses/viral-trigger-parkinsons)
[Post-Acute Viral Reservoir Hypothesis in Parkinson's Disease](/hypotheses/post-acute-viral-reservoir-parkinsons)
[Epigenetic Dysregulation Hypothesis in Parkinson's Disease](/hypotheses/epigenetic-dysregulation-parkinsons)
[Ethnicity-Specific Genetic Architecture Hypothesis in Parkinson's Disease](/hypotheses/ethnicity-specific-genetic-architecture-parkinsons)
[ER-Golgi Secretory Pathway Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/er-golgi-secretory-pathway-parkinsons)
[Glymphatic-Circadian Axis Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/glymphatic-circadian-axis-parkinsons)

Other Parkinson's Mechanisms

[Neural Oscillation Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/neural-oscillation-dysfunction-parkinsons)
[Non-Dopaminergic Neurotransmitter System Degeneration Hypothesis in Parkinson's Disease](/hypotheses/non-dopaminergic-neurotransmitter-parkinsons)
[Oligodendrocyte-Myelin Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/oligodendrocyte-myelin-dysfunction-parkinsons)
[Purinergic Signaling Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/purinergic-signaling-parkinsons)
[Regulated Necrosis Hypothesis in Parkinson's Disease](/hypotheses/regulated-necrosis-parkinsons)
[Sirtuin Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/sirtuin-dysfunction-parkinsons)
[Sirtuin Pathway Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/sirtuin-pathway-dysfunction-parkinsons)
[Stress Granule Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/stress-granule-dysfunction-parkinsons)
[Synaptic Vesicle Trafficking Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/synaptic-vesicle-trafficking-parkinsons)
[Wnt-Beta-Catenin Signaling Dysfunction Hypothesis in Parkinson's Disease](/hypotheses/wnt-beta-catenin-signaling-parkinsons)

FTD and ALS Hypotheses

[TBK1-Mediated Neuroinflammation Hypothesis: Autophagy Failure and Innate Immune Dysregulation in FTD/ALS](/hypotheses/tbk1-mediated-neuroinflammation-ftd-als)

Reference Pages

[Hypothesis Overview](/hypotheses/overview)
[Hypothesis Rankings](/hypotheses/rankings)

[Mechanisms](/mechanisms) — Molecular pathways and disease mechanisms
[Biomarkers](/biomarkers) — Disease markers and diagnostic indicators
[Therapeutics](/therapeutics) — Therapeutic approaches and treatments
[Researchers](/researchers) — Scientists developing hypotheses
[Genes](/genes) — Genetic risk factors
[Diseases](/diseases) — Disease-specific pages

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📗 Cite This Artifact

Hypotheses

Alzheimer's Disease Hypotheses

Alzheimer's Disease Hypotheses

Disease Model and Progression

Tau and Propagation

Cognitive and Network

Mouse Model and Mechanistic

Parkinson's Disease Hypotheses

Autophagy and Lysosomal Dysfunction

Mitochondrial and Metabolic

Neuroinflammation

Synuclein Propagation

Environmental and Systemic

Other Parkinson's Mechanisms

FTD and ALS Hypotheses

Reference Pages

See Also

💬 Discussion

📗 Cite This Artifact

Hypotheses

Alzheimer's Disease Hypotheses

Alzheimer's Disease Hypotheses

Disease Model and Progression

Tau and Propagation

Cognitive and Network

Mouse Model and Mechanistic

Parkinson's Disease Hypotheses

Autophagy and Lysosomal Dysfunction

Mitochondrial and Metabolic

Neuroinflammation

Synuclein Propagation

Environmental and Systemic

Other Parkinson's Mechanisms

FTD and ALS Hypotheses

Reference Pages

Related Sections

See Also

Related Hypotheses

💬 Discussion