Nicholas M. Kanaan

Analysis of isoform-specific tau aggregates suggests a common toxic mechanism involving similar pathological conformations and axonal transport inhibition.

Production of recombinant tau oligomers in vitro.

Pathogenic tau modifications occur in axons before the somatodendritic compartment in mossy fiber and Schaffer collateral pathways.

Peroxynitrite-induced nitrative and oxidative modifications alter tau filament formation.

Tyrosine nitration within the proline-rich region of Tau in Alzheimer's disease.

Characterization of prefibrillar Tau oligomers in vitro and in Alzheimer disease.

Ageing as a primary risk factor for Parkinson's disease: evidence from studies of non-human primates.

Pathogenic forms of tau inhibit kinesin-dependent axonal transport through a mechanism involving activation of axonal phosphotransferases.

Phosphorylation in the amino terminus of tau prevents inhibition of anterograde axonal transport.

Progression of tau pathology in cholinergic Basal forebrain neurons in mild cognitive impairment and Alzheimer's disease.

Heat shock protein 70 prevents both tau aggregation and the inhibitory effects of preexisting tau aggregates on fast axonal transport.

Axonal degeneration in Alzheimer's disease: when signaling abnormalities meet the axonal transport system.

Loss of functional alpha-synuclein: a toxic event in Parkinson's disease?

Recombinant adenoassociated virus 2/5-mediated gene transfer is reduced in the aged rat midbrain.

A method for combining RNAscope in situ hybridization with immunohistochemistry in thick free-floating brain sections and primary neuronal cultures.

The longitudinal transcriptomic response of the substantia nigra to intrastriatal 6-hydroxydopamine reveals significant upregulation of regeneration-associated genes.

Intrastriatal injection of pre-formed mouse α-synuclein fibrils into rats triggers α-synuclein pathology and bilateral nigrostriatal degeneration.

Gene Therapy Models of Alzheimer's Disease and Other Dementias.

Characterization of Early Pathological Tau Conformations and Phosphorylation in Chronic Traumatic Encephalopathy.

Quantitative and semi-quantitative measurements of axonal degeneration in tissue and primary neuron cultures.

Protein homeostasis gene dysregulation in pretangle-bearing nucleus basalis neurons during the progression of Alzheimer's disease.

Pathological conformations involving the amino terminus of tau occur early in Alzheimer's disease and are differentially detected by monoclonal antibodies.

Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport.

Pioglitazone prevents tau oligomerization.

Calcium dysregulation contributes to neurodegeneration in FTLD patient iPSC-derived neurons.

Soluble pre-fibrillar tau and β-amyloid species emerge in early human Alzheimer's disease and track disease progression and cognitive decline.

Progression of tau pathology within cholinergic nucleus basalis neurons in chronic traumatic encephalopathy: A chronic effects of neurotrauma consortium study.

Novel Non-phosphorylated Serine 9/21 GSK3β/α Antibodies: Expanding the Tools for Studying GSK3 Regulation.

Exposure of the Amino Terminus of Tau Is a Pathological Event in Multiple Tauopathies.

Aging and Parkinson's disease: Different sides of the same coin?

Aging Does Not Affect Axon Initial Segment Structure and Somatic Localization of Tau Protein in Hippocampal Neurons of Fischer 344 Rats.

Rationally Engineered AAV Capsids Improve Transduction and Volumetric Spread in the CNS.

Axonal Degeneration in Tauopathies: Disease Relevance and Underlying Mechanisms.

Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo.

Tau Oligomer Pathology in Nucleus Basalis Neurons During the Progression of Alzheimer Disease.

Tau Phosphorylation is Impacted by Rare AKAP9 Mutations Associated with Alzheimer Disease in African Americans.

Homocysteine Increases Tau Phosphorylation, Truncation and Oligomerization.

Tau Kinetics in Neurons and the Human Central Nervous System.

Lewy body-like alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration.

Correction to: Lewy body-like alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration.

Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer's disease.

Time course and magnitude of alpha-synuclein inclusion formation and nigrostriatal degeneration in the rat model of synucleinopathy triggered by intrastriatal α-synuclein preformed fibrils.

EFhd2 Affects Tau Liquid-Liquid Phase Separation.

Activity of the poly(A) binding protein MSUT2 determines susceptibility to pathological tau in the mammalian brain.

Rho-kinase ROCK inhibitors reduce oligomeric tau protein.

Tau and Axonal Transport Misregulation in Tauopathies.

A human induced pluripotent stem cell-derived cortical neuron human-on-a chip system to study Aβ and tau-induced pathophysiological effects on long-term potentiation.

Liquid-liquid phase separation induces pathogenic tau conformations in vitro.

Tau is not necessary for amyloid-β-induced synaptic and memory impairments.

TIA1 potentiates tau phase separation and promotes generation of toxic oligomeric tau.

Tau: A Signaling Hub Protein.

Neuronal and Glial Distribution of Tau Protein in the Adult Rat and Monkey.

EFhd2 brain interactome reveals its association with different cellular and molecular processes.

Frontotemporal Lobar Dementia Mutant Tau Impairs Axonal Transport through a Protein Phosphatase 1γ-Dependent Mechanism.

Clioquinol Decreases Levels of Phosphorylated, Truncated, and Oligomerized Tau Protein.

Mitochondrial oxidative stress contributes to the pathological aggregation and accumulation of tau oligomers in Alzheimer's disease.

Central role for p62/SQSTM1 in the elimination of toxic tau species in a mouse model of tauopathy.

Phosphomimetics at Ser199/Ser202/Thr205 in Tau Impairs Axonal Transport in Rat Hippocampal Neurons.

CRISPR screens in iPSC-derived neurons reveal principles of tau proteostasis.

Behavioral and neuropathological characterization over the adult lifespan of the human tau knock-in mouse.

Tau here, tau there, tau almost everywhere: Clarifying the distribution of tau in the adult CNS.