This index provides navigation for the Hypotheses section of NeuroWiki, covering research hypotheses about neurodegenerative disease mechanisms, disease progression models, and therapeutic approaches.
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)
[Cell-Type Specific TREM2 Upregulation in DAM Microglia](/hypothesis/h-seaad-51323624) — <span style="color:#81c784;font-weight:600">0.70</span> · Target: TREM2