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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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Thiamine-dependent processes and treatment strategies in neurodegeneration

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

2007

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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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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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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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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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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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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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Randomized clinical stroke trials in 2006

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

2008

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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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Glucose/mitochondria in neurological conditions

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

Blass, John P.

2002

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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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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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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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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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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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Brain metabolism and brain disease: Is metabolic deficiency the proximate cause of Alzheimer dementia?

Journal of neuroscience research, 2001-12, Vol.66 (5), p.851-856

Blass, John P.

2001

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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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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

Thiamine-dependent processes and treatment strategies in neurodegeneration

A New Approach to Treating Alzheimer's Disease

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

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

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

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

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

Randomized clinical stroke trials in 2006

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

Glucose/mitochondria in neurological conditions

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

Instruments for the Functional Assessment of Older Patients

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

Cerebrometabolic aspects of delirium in relationship to dementia

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”

Brain metabolism and brain disease: Is metabolic deficiency the proximate cause of Alzheimer dementia?

Mitochondrial enzymes in schizophrenia

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