Tiago F. Outeiro

This study develops a mouse model of Parkinson's disease by intranasal rotenone administration, showing progressive alpha-synuclein pathology from the olfactory bulb to other brain regions.

This study shows that specific Parkinson's disease-associated alpha-synuclein variants either enhance or impair condensate formation, highlighting divergent pathways in disease pathology.

This study investigates the interaction between LRRK1 and LRRK2, showing they modulate Rab7 activity and lysosomal exocytosis, with starvation reducing their interaction and impairing lysosomal homeostasis.

This study shows that Blm10/PA200 activates 20S proteasomes to degrade α-synuclein and resist inhibition, improving proteostasis in Parkinson's disease models.

This study shows that PPM1H knockout disrupts axonal autophagy and increases alpha-synuclein aggregation in neurons, linking LRRK2 hyperactivity to Parkinson disease pathology.

This study compares Tau oligomer properties in slowly and rapidly progressive Alzheimer's disease, finding distinct biochemical and proteomic profiles associated with different clinical progression rates.

This study shows that loss of CLN3 disrupts lysosomal lipid metabolism, leading to nuclear envelope lipid changes, DNA damage, and YAP1-driven apoptosis in Batten disease models.

This study shows that glycation of alpha-synuclein increases its aggregation and neuroinflammatory responses, linking type 2 diabetes and Parkinson's disease.

This study investigates how methylglyoxal and G93A SOD1 mutation affect TDP-43 interaction, showing increased cytosolic TDP-43 aggregation and reduced cell viability.

This study identifies molecular signatures of aging in the mouse brain through proteo-transcriptomic analysis, revealing changes in protein aggregation, mRNA relocalization, and translation efficiency linked to neurodegeneration.

This study overexpresses human alpha-synuclein in rodent glutamatergic neurons and finds no significant impairment in synaptic function.

This study examines how continuous and intermittent lead exposure affects synucleinopathies, finding increased aSyn inclusions and neurobehavioral impairments in animal models.

This study investigates the role of m6A RNA modification in synaptic function and ageing using a mouse model of synucleinopathy, finding age-related changes in m6A methylation of synaptic genes.

This study examines alpha-synuclein pathology in metachromatic leukodystrophy (MLD) brain tissue, finding seed-competent alpha-synuclein conformers in juvenile-onset cases, similar to Lewy body diseases.

This study shows DNA damage and repair dysfunction are linked to alpha-synuclein pathology in dementia with Lewy bodies, with DNA damage-derived material found within Lewy bodies.

This study identifies cofilin dysregulation as a mediator of α-synuclein-induced synaptic dysfunction in hippocampal neurons in synucleinopathy models.

This study models aSyn assemblies in living cells and shows that Sph1-aSyn interactions influence inclusion formation, morphology, and localization, providing insights into protein aggregation and potential therapeutic strategies.

This study shows that intracellular Aβ correlates with AT-8 phosphorylated tau in frontal cortex tissue from non-AD and AD brains, supporting the revised amyloid cascade hypothesis.

The paper investigates whether Lewy bodies form due to impaired autophagy and mitochondrial dysfunction, finding enriched autophagic markers and proteomic evidence of aggresome-like pathways in Lewy bodies.

The paper shows that alpha-synuclein oligomers activate NFAT, leading to neuronal toxicity and synaptic loss, which can be reversed by NFAT inhibitors.

The paper investigates sensory system aberrations in a Parkinson's Disease mouse model using fMRI and finds neural origins for observed deficits.

This study shows that glycation worsens Parkinson's-like symptoms in mice by enhancing glutamatergic signaling and causing dopaminergic neuron loss.

This study compares the release and effects of alpha-synuclein, Tau, and huntingtin in neuronal cells, showing similar release pathways and impacts on neuronal activity and inflammation.

The paper characterizes ectosomes and exosomes proteomes and shows they modulate neuronal activity differently.

This study identifies DNA methylation and hydroxymethylation changes in dopaminergic neurons overexpressing alpha-synuclein variants, linking them to altered gene expression in PD-related pathways.

This study uses super-resolution microscopy to examine the molecular structure of alpha-synuclein inclusions in cell models and human brain tissue, revealing conserved patterns and shapes.

This study shows doxycycline reduces α-synuclein aggregation and oxidative stress in vitro and in vivo, suggesting it could treat synucleinopathies like Parkinson's disease.

The paper evaluates pharmacological modulators of α-synuclein and tau aggregation and internalization, identifying compounds that reduce their aggregation and spread.

This study shows that Hsp27 reduces glycation-induced toxicity and aggregation of α-synuclein in cellular models.

This study shows that protein phosphatase 1 (PP1) regulates huntingtin exon 1 (HTTex1) aggregation and toxicity by modulating phosphorylation at T3.