David Koss

Newcastle University

United Kingdom

Research Interests

Explore related searches

Professors in United Kingdom

Contact this professor

Get a free first email built on one of their papers, ready for you to edit and send yourself.

Articles (13)

Year:

2025

Year:

2024

Year:

2024

Year:

2022

Year:

2022

Year:

2022

Year:

2021

Year:

2021

Year:

2021

Year:

2020

Year:

2020

Year:

2020

Year:

2020

Collaborators (6)

Flaviano Giorgini

University of Leicester

UNITED KINGDOM

View details

Johannes Attems

Professor of Neuropathology, Honorary Consultant Pathologist

Newcastle University

UNITED KINGDOM

View details

Daniel Erskine

Newcastle University

UNITED KINGDOM

View details

Minna Oinas

University of Helsinki

FINLAND

View details

Liisa Myllykangas

University of Helsinki

FINLAND

View details

Antonio Domínguez Meijide

Universidade de Santiago de Compostela

SPAIN

View details

ApplyKite TwinLearns as you apply

Make your next move.

Prepare your application

Review drafts before you send them.

David Koss

Research Interests

Explore related searches

Contact this professor

Articles (13)

A reciprocal relationship between markers of genomic DNA damage and alpha-synuclein pathology in dementia with Lewy bodies.

Altered hippocampal doublecortin expression in Parkinson's disease

Regional AT-8 reactive tau species correlate with intracellular Aβ levels in cases of low AD neuropathologic change

Blood mRNA Expression in Alzheimer's Disease and Dementia With Lewy Bodies

Prion-like α-synuclein pathology in the brain of infants with Krabbe disease

Nuclear alpha-synuclein is present in the human brain and is modified in dementia with Lewy bodies

Lipids, lysosomes and mitochondria: insights into Lewy body formation from rare monogenic disorders.

Dysfunction of RAB39B‐Mediated Vesicular Trafficking in Lewy Body Diseases

Frontal white matter lesions in Alzheimer’s disease are associated with both small vessel disease and AD-associated cortical pathology

Synucleinopathies: Where we are and where we need to go

Concomitant LATE-NC in Alzheimer's disease is not associated with increased tau or amyloid-β pathological burden.

RAB39B is redistributed in dementia with Lewy bodies and is sequestered within aβ plaques and Lewy bodies.

Synaptic Loss, ER Stress and Neuro-Inflammation Emerge Late in the Lateral Temporal Cortex and Associate with Progressive Tau Pathology in Alzheimer's Disease.

Collaborators (6)

Flaviano Giorgini

Johannes Attems

Daniel Erskine

Minna Oinas

Liisa Myllykangas

Antonio Domínguez Meijide

Make your next move.