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Cause and consequence: Mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases

Biochimica et biophysica acta, 2010-01, Vol.1802 (1), p.122-134

2010

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Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications

Annals of neurology, 2005-05, Vol.57 (5), p.695-703

2005

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Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology

The Journal of experimental medicine, 2004-07, Vol.200 (2), p.211-222

2004

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Thiamine-dependent processes and treatment strategies in neurodegeneration

Antioxidants & redox signaling, 2007-10, Vol.9 (10), p.1605-1620

2007

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The Mitochondrial Spiral: An Adequate Cause of Dementia in the Alzheimer's Syndrome

Annals of the New York Academy of Sciences, 2000-12, Vol.924 (1), p.170-183

BLASS, JOHN P.

2000

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The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration

Molecular neurobiology, 2005, Vol.31 (1-3), p.43-64

2005

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A New Approach to Treating Alzheimer's Disease

Annals of the New York Academy of Sciences, 2008-12, Vol.1147 (1), p.122-128

Blass, John P.

2008

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Instruments for the Functional Assessment of Older Patients

The New England journal of medicine, 1990-04, Vol.322 (17), p.1207-1214

1990

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Cerebrometabolic aspects of delirium in relationship to dementia

Dementia and geriatric cognitive disorders, 1999-09, Vol.10 (5), p.335-338

1999

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Alzheimer's disease and Alzheimer's dementia: distinct but overlapping entities

Neurobiology of aging, 2002-11, Vol.23 (6), p.1077-1084

Blass, John P

2002

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Increased levels of γ-glutamylamines in Huntington disease CSF

Journal of neurochemistry, 2008-07, Vol.106 (1), p.37-44

2008

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The α-ketoglutarate dehydrogenase complex in neurodegeneration

Neurochemistry International, 2000-02, Vol.36 (2), p.97-112

2000

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Cerebrometabolic abnormalities in Alzheimer's disease

Neurological research (New York), 2003-09, Vol.25 (6), p.556-566

Blass, John P.

2003

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The role of the metabolic lesion in Alzheimer's disease

Journal of Alzheimer's disease, 2002-06, Vol.4 (3), p.225-232

2002

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Absence of Vascular Dementia in an Autopsy Series from a Dementia Clinic

Journal of the American Geriatrics Society (JAGS), 1998-05, Vol.46 (5), p.597-604

1998

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Transglutaminase Activity Is Present in Highly Purified Nonsynaptosomal Mouse Brain and Liver Mitochondria

Biochemistry (Easton), 2005-05, Vol.44 (21), p.7830-7843

2005

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Correlations of disability and biologic alterations in Alzheimer brain and test of significance by a therapeutic trial in humans

Journal of Alzheimer's disease, 2006-07, Vol.9 (2), p.207-218

2006

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N ε ‐(γ‐l‐Glutamyl)‐l‐lysine (GGEL) is increased in cerebrospinal fluid of patients with Huntington's disease

Journal of neurochemistry, 2001-12, Vol.79 (5), p.1109-1112

2001

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Mitochondrial aconitase is a transglutaminase 2 substrate: transglutamination is a probable mechanism contributing to high-molecular-weight aggregates of aconitase and loss of aconitase activity in Huntington disease brain

Neurochemical research, 2005-10, Vol.30 (10), p.1245-1255

2005

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Glucose/mitochondria in neurological conditions

Glucose Metabolism in the Brain, 2002, Vol.51, p.325-376

2002

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Cross linking of polyglutamine domains catalyzed by tissue transglutaminase is greatly favored with pathological-length repeats: does transglutaminase activity play a role in (CAG)n/Qn-expansion diseases

Neurochemistry international, 2002, Vol.40 (1), p.53-67

2002

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Commentary on “Diagnosis of Alzheimer’s disease: Two decades of progress.” Perspectives on “Perspectives”

Alzheimer's & dementia, 2005-10, Vol.1 (2), p.124-125

Blass, John P.

2005

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Mitochondrial enzymes in schizophrenia

Journal of molecular neuroscience, 2004-01, Vol.24 (2), p.315-322

2004

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Randomized clinical stroke trials in 2006

Current vascular pharmacology, 2008-01, Vol.6 (1), p.61-66

2008

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Admission C-reactive protein does not predict functional outcomes in patients with strokes in a subacute rehabilitation unit

American journal of physical medicine & rehabilitation, 2008-09, Vol.87 (9), p.731-739

2008

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Cause and consequence: Mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases

Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications

Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology

Thiamine-dependent processes and treatment strategies in neurodegeneration

The Mitochondrial Spiral: An Adequate Cause of Dementia in the Alzheimer's Syndrome

The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration

A New Approach to Treating Alzheimer's Disease

Instruments for the Functional Assessment of Older Patients

Cerebrometabolic aspects of delirium in relationship to dementia

Alzheimer's disease and Alzheimer's dementia: distinct but overlapping entities

Increased levels of γ-glutamylamines in Huntington disease CSF

The α-ketoglutarate dehydrogenase complex in neurodegeneration

Cerebrometabolic abnormalities in Alzheimer's disease

The role of the metabolic lesion in Alzheimer's disease

Absence of Vascular Dementia in an Autopsy Series from a Dementia Clinic

Transglutaminase Activity Is Present in Highly Purified Nonsynaptosomal Mouse Brain and Liver Mitochondria

Correlations of disability and biologic alterations in Alzheimer brain and test of significance by a therapeutic trial in humans

N ε ‐(γ‐l‐Glutamyl)‐l‐lysine (GGEL) is increased in cerebrospinal fluid of patients with Huntington's disease

Mitochondrial aconitase is a transglutaminase 2 substrate: transglutamination is a probable mechanism contributing to high-molecular-weight aggregates of aconitase and loss of aconitase activity in Huntington disease brain

Glucose/mitochondria in neurological conditions

Cross linking of polyglutamine domains catalyzed by tissue transglutaminase is greatly favored with pathological-length repeats: does transglutaminase activity play a role in (CAG)n/Qn-expansion diseases

Commentary on “Diagnosis of Alzheimer’s disease: Two decades of progress.” Perspectives on “Perspectives”

Mitochondrial enzymes in schizophrenia

Randomized clinical stroke trials in 2006

Admission C-reactive protein does not predict functional outcomes in patients with strokes in a subacute rehabilitation unit

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