Tau is required for progressive synaptic and memory deficits in a transgenic mouse model of α-synucleinopathy

Bidirectional modulation of Alzheimer phenotype by alpha-synuclein in mice and primary neurons

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α-Synuclein Oligomers Induce a Unique Toxic Tau Strain

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Are dementia with Lewy bodies and Parkinson’s disease dementia the same disease?

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Tau oligomers mediate α-synuclein toxicity and can be targeted by immunotherapy

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Nav1.1-Overexpressing Interneuron Transplants Restore Brain Rhythms and Cognition in a Mouse Model of Alzheimer’s Disease

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The Genetics of Dementia with Lewy Bodies: Current Understanding and Future Directions

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A53T mutant alpha-synuclein induces tau dependent postsynaptic impairment independent of neurodegenerative changes

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Cognitive and Pathological Influences of Tau Pathology in Lewy Body Disorders

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Cellular prion protein neither binds to alpha-synuclein oligomers nor mediates their detrimental effects

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Global, regional, and national burden of Parkinson's disease, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

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Relative Incidence of Seizures and Myoclonus in Alzheimer’s Disease, Dementia with Lewy Bodies, and Frontotemporal Dementia

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α-synuclein interacts with PrPC to induce cognitive impairment through mGluR5 and NMDAR2B

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Animal models of α-synucleinopathy for Parkinson disease drug development

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Frontotemporal dementia as the presenting phenotype of p.A53T mutation carriers in the alpha-synuclein gene

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Selective lowering of synapsins induced by oligomeric α-synuclein exacerbates memory deficits

(2017) Megan E. Larson et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

The amyloid-β oligomer Aβ*56 induces specific alterations in neuronal signaling that lead to tau phosphorylation and aggregation

(2017) Fatou Amar et al.   Science Signaling

The amyloid-β oligomer Aβ*56 induces specific alterations in neuronal signaling that lead to tau phosphorylation and aggregation

(2017) Fatou Amar et al.   Science Signaling

Parkinson disease

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Meta-analysis of synaptic pathology in Alzheimer's disease reveals selective molecular vesicular machinery vulnerability

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Hippocampal α-Synuclein in Dementia with Lewy Bodies Contributes to Memory Impairment and Is Consistent with Spread of Pathology

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Soluble Conformers of A  and Tau Alter Selective Proteins Governing Axonal Transport

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Network abnormalities and interneuron dysfunction in Alzheimer disease

(2016) Jorge J. Palop et al.   NATURE REVIEWS NEUROSCIENCE

Hippocampal volumes predict risk of dementia with Lewy bodies in mild cognitive impairment

(2016) Kejal Kantarci et al.   NEUROLOGY

Induction of de novo α-synuclein fibrillization in a neuronal model for Parkinson’s disease

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Pathological Interface Between Oligomeric Alpha-Synuclein and Tau in Synucleinopathies

(2015) Urmi Sengupta et al.   BIOLOGICAL PSYCHIATRY

Effects of Serine 129 Phosphorylation on α-Synuclein Aggregation, Membrane Association, and Internalization

(2015) Filsy Samuel et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Hippocampal Lewy pathology and cholinergic dysfunction are associated with dementia in Parkinson’s disease

(2014) Hélène Hall et al.   BRAIN

Tau phosphorylation and tau mislocalization mediate soluble Aβ oligomer-induced AMPA glutamate receptor signaling deficits

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α-Synuclein assembles into higher-order multimers upon membrane binding to promote SNARE complex formation

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Confluence of α-Synuclein, Tau, and β-Amyloid Pathologies in Dementia With Lewy Bodies

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Properties of native brain α-synuclein

(2013) Jacqueline Burré et al.   NATURE

Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies

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Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein

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Behavioral Characterization of A53T Mice Reveals Early and Late Stage Deficits Related to Parkinson’s Disease

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Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model

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Cognitive deficits in a mouse model of pre-manifest Parkinson’s disease

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Identification of oligomers at early stages of tau aggregation in Alzheimer's disease

(2012) Cristian A. Lasagna-Reeves et al.   FASEB JOURNAL

Accumulation of Toxic  -Synuclein Oligomer within Endoplasmic Reticulum Occurs in  -Synucleinopathy In Vivo

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The Complex PrPc-Fyn Couples Human Oligomeric A  with Pathological Tau Changes in Alzheimer's Disease

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Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons

(2012) Ji Won Um et al.   NATURE NEUROSCIENCE

A Progressive Mouse Model of Parkinson’s Disease: The Thy1-aSyn (“Line 61”) Mice

(2012) Marie-Francoise Chesselet et al.   Neurotherapeutics

Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model

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Soluble Aβ oligomer production and toxicity

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 -Syn Suppression Reverses Synaptic and Memory Defects in a Mouse Model of Dementia with Lewy Bodies

(2011) Y. Lim et al.   JOURNAL OF NEUROSCIENCE

Amyloid- /Fyn-Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease

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Ablation of Cellular Prion Protein Does Not Ameliorate Abnormal Neural Network Activity or Cognitive Dysfunction in the J20 Line of Human Amyloid Precursor Protein Transgenic Mice

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Resistance to MPTP-Neurotoxicity in α-Synuclein Knockout Mice Is Complemented by Human α-Synuclein and Associated with Increased β-Synuclein and Akt Activation

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Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models

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Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein

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Mice expressing the A53T mutant form of human alpha-synuclein exhibit hyperactivity and reduced anxiety-like behavior

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(2010) Jose A Obeso et al.   NATURE MEDICINE

Increased Expression of α-Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering after Endocytosis

(2010) Venu M. Nemani et al.   NEURON

Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration

(2010) Brian R. Hoover et al.   NEURON

Tau Reduction Prevents Aβ-Induced Defects in Axonal Transport: Fig. 1

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 -Synuclein Promotes SNARE-Complex Assembly in Vivo and in Vitro

(2010) J. Burre et al.   SCIENCE

Intermediate- and long-term recognition memory deficits in Tg2576 mice are reversed with acute calcineurin inhibition

(2009) Giulio Taglialatela et al.   BEHAVIOURAL BRAIN RESEARCH

Detection of elevated levels of soluble  -synuclein oligomers in post-mortem brain extracts from patients with dementia with Lewy bodies

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Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease

(2009) Binggui Sun et al.   Cell Stem Cell

Forebrain overexpression of α-synuclein leads to early postnatal hippocampal neuron loss and synaptic disruption

(2009) Youngshin Lim et al.   EXPERIMENTAL NEUROLOGY

Amyloid  -Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy

(2009) R. Minkeviciene et al.   JOURNAL OF NEUROSCIENCE

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers

(2009) Juha Laurén et al.   NATURE

Synaptic Depression and Aberrant Excitatory Network Activity in Alzheimer’s Disease: Two Faces of the Same Coin?

(2009) Jorge J. Palop et al.   NEUROMOLECULAR MEDICINE

Clinical, neuropathological and genotypic variability in SNCA A53T familial Parkinson’s disease

(2008) K. Markopoulou et al.   ACTA NEUROPATHOLOGICA

Dementia in Parkinsonʼs disease

(2008) Dag Aarsland et al.   CURRENT OPINION IN NEUROLOGY

The Sydney multicenter study of Parkinson's disease: The inevitability of dementia at 20 years

(2008) Mariese A. Hely et al.   MOVEMENT DISORDERS

Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease

(2008) Rene O Sanchez-Mejia et al.   NATURE NEUROSCIENCE

Invited Article: Nervous system pathology in sporadic Parkinson disease

(2008) H. Braak et al.   NEUROLOGY

Dementia and visual hallucinations associated with limbic pathology in Parkinson's disease

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