Sidney Strickland

Tissue plasminogen activator in nervous system function and dysfunction.

Localization and regulation of the tissue plasminogen activator-plasmin system in the hippocampus.

Fibrin inhibits peripheral nerve remyelination by regulating Schwann cell differentiation.

Nervous system pathology: the fibrin perspective.

Tissue plasminogen activator and seizures: a clot-buster's secret life.

Tissue plasminogen activator in the amygdala is critical for stress-induced anxiety-like behavior.

Fibrin is a regulator of Schwann cell migration after sciatic nerve injury in mice.

The hippocampal laminin matrix is dynamic and critical for neuronal survival.

The possible role of tissue-type plasminogen activator (tPA) and tPA blockers in the pathogenesis and treatment of Alzheimer's disease.

The tissue plasminogen activator-plasminogen proteolytic cascade accelerates amyloid-beta (Abeta) degradation and inhibits Abeta-induced neurodegeneration.

Laminin gamma1 is critical for Schwann cell differentiation, axon myelination, and regeneration in the peripheral nerve.

Fibrin depletion decreases inflammation and delays the onset of demyelination in a tumor necrosis factor transgenic mouse model for multiple sclerosis.

Tissue plasminogen activator promotes the effects of corticotropin-releasing factor on the amygdala and anxiety-like behavior.

Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors.

Tissue plasminogen activator in central nervous system physiology and pathology.

Schwann cell-specific ablation of laminin gamma1 causes apoptosis and prevents proliferation.

Tissue plasminogen activator and plasminogen mediate stress-induced decline of neuronal and cognitive functions in the mouse hippocampus.

The plasminogen activator system modulates sympathetic nerve function.

Peripheral regeneration.

Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimer's disease.

Modulation of NR2B-regulated contextual fear in the hippocampus by the tissue plasminogen activator system.

Key role of tissue plasminogen activator in neurovascular coupling.

Disruption of laminin in the peripheral nervous system impedes nonmyelinating Schwann cell development and impairs nociceptive sensory function.

Proteolytic fragments of laminin promote excitotoxic neurodegeneration by up-regulation of the KA1 subunit of the kainate receptor.

Cortical deficiency of laminin gamma1 impairs the AKT/GSK-3beta signaling pathway and leads to defects in neurite outgrowth and neuronal migration.

Tissue plasminogen activator modulates the cellular and behavioral response to cocaine.

Laminin is required for Schwann cell morphogenesis.

Plasmin-mediated degradation of laminin gamma-1 is critical for ethanol-induced neurodegeneration.

Maximum-entropy network analysis reveals a role for tumor necrosis factor in peripheral nerve development and function.

Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease.

Involvement of tissue plasminogen activator in stress responsivity during acute cocaine withdrawal in mice.

Alzheimer's disease peptide beta-amyloid interacts with fibrinogen and induces its oligomerization.

Mesenchymal stem cells facilitate axon sorting, myelination, and functional recovery in paralyzed mice deficient in Schwann cell-derived laminin.

Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice.

Renal collecting system growth and function depend upon embryonic γ1 laminin expression.

Aβ delays fibrin clot lysis by altering fibrin structure and attenuating plasminogen binding to fibrin.

Schwann cell myelination requires integration of laminin activities.

Fibrinogen and altered hemostasis in Alzheimer's disease.

The GluK4 kainate receptor subunit regulates memory, mood, and excitotoxic neurodegeneration.

The APOE ɛ4/ɛ4 genotype potentiates vascular fibrin(ogen) deposition in amyloid-laden vessels in the brains of Alzheimer's disease patients.

Ablation of astrocytic laminin impairs vascular smooth muscle cell function and leads to hemorrhagic stroke.

Astrocytic laminin regulates pericyte differentiation and maintains blood brain barrier integrity.

Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain.

A novel Aβ-fibrinogen interaction inhibitor rescues altered thrombosis and cognitive decline in Alzheimer's disease mice.

The cellular origin of laminin determines its role in blood pressure regulation.

Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration.

Activation of the factor XII-driven contact system in Alzheimer's disease patient and mouse model plasma.

Chronic Hypertension Leads to Neurodegeneration in the TgSwDI Mouse Model of Alzheimer's Disease.

The Alzheimer's disease peptide β-amyloid promotes thrombin generation through activation of coagulation factor XII.

Hyperhomocysteinemia exacerbates Alzheimer's disease pathology by way of the β-amyloid fibrinogen interaction.

Laminin regulates PDGFRβ(+) cell stemness and muscle development.

A possible new role for Aβ in vascular and inflammatory dysfunction in Alzheimer's disease.

Biochemical and structural analysis of the interaction between β-amyloid and fibrinogen.

Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice.

Interactions of β-amyloid peptide with fibrinogen and coagulation factor XII may contribute to Alzheimer's disease.

Fibrinogen in the Nervous System: Glia Beware.

Aminopyrimidine Class Aggregation Inhibitor Effectively Blocks Aβ-Fibrinogen Interaction and Aβ-Induced Contact System Activation.

Abnormal clotting of the intrinsic/contact pathway in Alzheimer disease patients is related to cognitive ability.

Blood-derived plasminogen drives brain inflammation and plaque deposition in a mouse model of Alzheimer's disease.

A novel detection method of cleaved plasma high-molecular-weight kininogen reveals its correlation with Alzheimer's pathology and cognitive impairment.