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Article ; Online: Neurodegeneration: 2023 update.

Crary, John F

Free neuropathology

2023 Volume 4

Abstract: This paper reviews ten highly impactful studies published in the previous year selected by the author from the neurodegenerative neuropathology literature. As in previous years, the focus is to highlight human tissue-based experimentation most relevant ... ...

Abstract	This paper reviews ten highly impactful studies published in the previous year selected by the author from the neurodegenerative neuropathology literature. As in previous years, the focus is to highlight human tissue-based experimentation most relevant to neuropathologists. A concerted effort was made to balance the selected studies across disease categories, approaches, and methodologies to capture the breadth of the research landscape. Studies include an integrated proteomic and transcriptomic study of Alzheimer disease (AD) and new consensus diagnostic neuropathological criteria for progressive supranuclear palsy. A number of studies looking at TAR DNA-binding protein 43 (TDP-43) are highlighted. One examined interaction between AD and limbic age-related TDP-43 encephalopathy (LATE) and yet another demonstrated how TDP-43 represses cryptic exon inclusion in
Language	English
Publishing date	2023-09-04
Publishing country	Germany
Document type	Journal Article
ISSN	2699-4445
ISSN (online)	2699-4445
DOI	10.17879/freeneuropathology-2023-4899
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Article ; Online: Neurodegeneration: 2022 update.

Crary, John F

Free neuropathology

2022 Volume 3

Abstract: Here, we review a collection of recent manuscripts and research trends on the neuropathology of neurodegeneration that are considered by the author to be among the potentially most impactful. To the greatest extent possible, we chose to focus on ... ...

Abstract	Here, we review a collection of recent manuscripts and research trends on the neuropathology of neurodegeneration that are considered by the author to be among the potentially most impactful. To the greatest extent possible, we chose to focus on histopathological studies that are most relevant to experimental and diagnostic neuropathology. While there has been an abundance of important recent discoveries and developments in neurodegenerative disease research, there was a deliberate effort here to provide balance to prevent disease categories and experimental approaches from overshadowing the others. The result is a diverse series of outstanding studies, together showing the landscape of progress across neurodegenerative disorders. One is a stereological study examining dystrophic microglia in aging. We highlight the first large genetic study of primary age-related tauopathy, showing convergence and divergence from classical Alzheimer's disease. There were further advances in the neuropathological criteria and staging of chronic traumatic encephalopathy. Links suggesting a causal role for
Language	English
Publishing date	2022-05-10
Publishing country	Germany
Document type	Journal Article
ISSN	2699-4445
ISSN (online)	2699-4445
DOI	10.17879/freeneuropathology-2022-3866
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Article ; Online: Neurodegeneration: 2021 update.

Crary, John F

Free neuropathology

2021 Volume 2

Abstract: This article reviews a collection of manuscripts in the field of neurodegenerative disease chosen from what are considered by the author to be among the 10 most important and potentially impactful topics or research trends of 2020 relevant to the field ... ...

Abstract	This article reviews a collection of manuscripts in the field of neurodegenerative disease chosen from what are considered by the author to be among the 10 most important and potentially impactful topics or research trends of 2020 relevant to the field of experimental and diagnostic neuropathology. A deliberate effort was made to provide balance among disease categories covered. The result is a varied selection that includes not just individual papers but also research topics and trends. The association of COVID-19 with longer-term neurological symptoms has launched a research trend fueled by speculation that the SARS-CoV-2 might trigger neurodegenerative changes. The onslaught of transcriptomic studies has begun to give way to proteomics, with three transformative studies published examining glial contributions to Alzheimer disease, cerebral atherosclerosis in cognitive decline, and the complex sequence of post-translational modifications of the tau protein. Plasma biomarkers for Alzheimer disease have continued to make rapid advances, especially around highly sensitive assays capable of detecting different forms of abnormal hyperphosphorylated tau in peripheral blood. Two studies using cryo-electron microscopy showed the power of the approach by continuing to elucidate the diversity of filamentous tau inclusions, and a third study gave the first glimpse of α-synuclein aggregates at near atomic resolution. Another study continued to delineate how different α-synuclein conformers ("strains") target specific brain regions and lead to neurodegeneration. In Huntington's disease, we saw compelling molecular data showing how cells adapt to endoplasmic reticulum stress through the unfolded protein response. Finally, the role of astrocytes in chronic traumatic encephalopathy has emerged as a critical area of interest.
Language	English
Publishing date	2021-04-21
Publishing country	Germany
Document type	Journal Article
ISSN	2699-4445
ISSN (online)	2699-4445
DOI	10.17879/freeneuropathology-2021-3317
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Article ; Online: Top ten discoveries of the year: Neurodegeneration.

Crary, John F

Free neuropathology

2020 Volume 1

Abstract: As we embark on a new year of scientific inquiry in neurodegenerative disease research, it is helpful to take a look back and consider the contributions in the field with the potential to be the most impactful. The purpose of this review is to highlight ... ...

Abstract	As we embark on a new year of scientific inquiry in neurodegenerative disease research, it is helpful to take a look back and consider the contributions in the field with the potential to be the most impactful. The purpose of this review is to highlight recent advances in 2019 which have the potential to be transformative in the field of neurodegenerative neuropathology. Substantive scientific progress rarely occurs as a "eureka moment", and when possible, we opted to highlight collaborative efforts and research trends. We also included groundbreaking methodologies and tools. The generous increases in federal funding in the United States and elsewhere have massively expanded the total number of active programs researching Alzheimer's disease. This exacerbates an imbalance, and an effort was made to highlight innovations across disease categories, and not to permit dementia to crowd out movement disorders, motor neuron disease, ataxias, etc. Thus, our overall goal was to highlight some of the most important discoveries, tools or methods that we feel will most likely directly enhance our ability to understand and diagnose neurodegenerative brain diseases. Given space limitations and the targeted readership of this journal, we selected ten topics most relevant to neuropathologists and clinical neuroscientists: 1. A new neurodegenerative disease category, 2. A new approach to probing gene expression on the single cell level, 3. A new approach merging histology and gene expression profiling, 4. A new computational approach using deep machine learning and computer vision, 5. A neuropathological substrate for sleep disturbance in Alzheimer's disease, 6. A candidate pathogenic agent for Alzheimer's disease, 7. A comprehensive approach to morphometric analysis of cerebellar neurodegeneration, 8. The strongest evidence yet linking neurodegeneration to contact sports, 9. Mounting evidence for gut to central nervous system transmission in Parkinson's disease, and 10. A spotlight on glia in Huntington's disease.
Language	English
Publishing date	2020-04-08
Publishing country	Germany
Document type	Journal Article
ISSN	2699-4445
ISSN (online)	2699-4445
DOI	10.17879/freeneuropathology-2020-2634
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Article ; Online: Chronic Traumatic Encephalopathy and Neuropathological Comorbidities.

Stein, Thor D / Crary, John F

Seminars in neurology

2020 Volume 40, Issue 4, Page(s) 384–393

Abstract: With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of ... ...

Abstract	With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of many neurodegenerative diseases, including chronic traumatic encephalopathy (CTE), Alzheimer's disease, Lewy body disease, and amyotrophic lateral sclerosis, it is becoming critical to understand the relationship and interactions between these pathologies. In fact, comorbid pathology is common in CTE and likely influenced by both age and the severity and type of exposure to RHI as well as underlying genetic predisposition. Here, we review the major comorbid pathologies seen with CTE and in former contact sports athletes and discuss what is known about the associations between RHI, age, and the development of neuropathologies. In addition, we examine the distinction between CTE and age-related pathology including primary age-related tauopathy and age-related tau astrogliopathy.
MeSH term(s)	Alzheimer Disease/epidemiology ; Alzheimer Disease/pathology ; Amyotrophic Lateral Sclerosis/epidemiology ; Amyotrophic Lateral Sclerosis/pathology ; Chronic Traumatic Encephalopathy/epidemiology ; Chronic Traumatic Encephalopathy/pathology ; Comorbidity ; Humans ; Lewy Body Disease/epidemiology ; Lewy Body Disease/pathology ; Tauopathies/epidemiology ; Tauopathies/pathology
Language	English
Publishing date	2020-06-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713628
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Article: Primary age-related tauopathy and the amyloid cascade hypothesis: the exception that proves the rule?

Crary, John F

Journal of neurology & neuromedicine

2016 Volume 1, Issue 6, Page(s) 53–57

Abstract: Extensive data supports the amyloid cascade hypothesis, which states that Alzheimer's disease (AD) stems from neurotoxic forms of the amyloid-beta (Aβ) peptide. But the poor correlation between Aβ plaques and neurodegeneration/cognitive impairment, the ... ...

Abstract	Extensive data supports the amyloid cascade hypothesis, which states that Alzheimer's disease (AD) stems from neurotoxic forms of the amyloid-beta (Aβ) peptide. But the poor correlation between Aβ plaques and neurodegeneration/cognitive impairment, the spaciotemporal disparity between Aβ and tau pathology, and the disappointing results following several large clinical trials using Aβ-targeting agents are inconsistent with this explanation. The most perplexing inconsistency is the existence of AD-type dementia patients that develop abundant neurofibrillary tangles that are indistinguishable from those in early to moderate-stage AD in the absence of compelling evidence of amyloid toxicity. This neuropathological phenotype, which is distinct from other diseases with tangles, represents a conceptual disconnect, because it does not fall within any previously established category of tauopathy and ostensibly invalidates the amyloid cascade hypothesis. Instead, recent efforts have led to consensus criteria for a new alternative diagnostic category, which presupposes that these tangle-only dementia patients represent extreme examples of a distinct primary age-related tauopathy (PART) that is universally observed, albeit to varying degrees, in the aging brain. The cause of PART is unknown, but sufficient evidence exists to hypothesize that it stems from an Aβ-independent mechanism, such as mechanical injury. Should the PART hypothesis withstand further experimental testing, it would represent a shift in the way a subset of subjects with AD neuropathological change are classified and has the potential to focus and reaffirm the amyloid cascade hypothesis.
Language	English
Publishing date	2016-06-28
Publishing country	United States
Document type	Journal Article
ISSN	2572-942X
ISSN	2572-942X
DOI	10.29245/2572.942x/2016/6.1059
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Article ; Online: Cognitive Performance as a Function of MAPT Haplotype: A Prospective Longitudinal Study of an Essential Tremor Cohort.

Ghanem, Ali / Berry, Diane S / Farrell, Kurt / Cosentino, Stephanie / Crary, John F / Louis, Elan D

Tremor and other hyperkinetic movements (New York, N.Y.)

2023 Volume 13, Page(s) 19

Abstract: Background: Cognitive impairment is a feature of essential tremor (ET). There are no studies of the genetic drivers of this association. We examined whether the microtubule-associated protein tau (MAPT) H1 haplotype is associated with cognitive ... ...

Abstract	Background: Cognitive impairment is a feature of essential tremor (ET). There are no studies of the genetic drivers of this association. We examined whether the microtubule-associated protein tau (MAPT) H1 haplotype is associated with cognitive performance in ET. Methods: ET cases genotyped for the MAPT H1 and H2 haplotypes completed a battery of neuropsychological tests at baseline and four follow-up evaluations. Chi-square, t-tests, and analyses of covariance examined associations between the presence of the MAPT H1 haplotype, cognitive diagnoses of normal, mild cognitive impairment (MCI), and dementia, and performance in specific cognitive domains. Results: We observed no evidence of cognitive differences as a function of the presence of the MAPT H1 haplotype. Specifically, cases with (n = 57) and without (n = 42) this haplotype did not differ with respect to the prevalence of diagnoses of MCI or dementia, Discussion: The study in an ET cohort revealed no influence of MAPT haplotypes on cognitive performance. This study serves as a valuable foundation for future studies to expand our understanding of the genetic drivers of cognitive impairment in ET. Highlights: This study found no evidence of cognitive differences between individuals with and without the MAPT H1 haplotype. Our work provides a valuable foundation for future work to expand our knowledge of the genetic drivers of cognitive impairment in ET.
MeSH term(s)	Humans ; Longitudinal Studies ; Prospective Studies ; Essential Tremor/genetics ; Dementia/genetics ; Cognition ; tau Proteins/genetics
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2023-05-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2674453-3
ISSN	2160-8288 ; 2160-8288
ISSN (online)	2160-8288
ISSN	2160-8288
DOI	10.5334/tohm.768
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Article ; Online: Neuronal accumulation of hyperphosphorylated tau protein predicts stable memory impairment in people living with HIV.

Gonzalez, Jairo / Wilson, Alyssa / Byrd, Desiree / Cortes, Etty P / Crary, John F / Morgello, Susan

AIDS (London, England)

2023 Volume 37, Issue 8, Page(s) 1247–1256

Abstract: Objectives: As lifespans increase in people with HIV (PWH), there is concern that age-related neurodegenerative disorders may contribute to cognitive decline. We asked whether brain accumulation of Alzheimer's disease (AD)-associated proteins amyloid- ... ...

Abstract	Objectives: As lifespans increase in people with HIV (PWH), there is concern that age-related neurodegenerative disorders may contribute to cognitive decline. We asked whether brain accumulation of Alzheimer's disease (AD)-associated proteins amyloid-beta (Aβ) and hyperphosphorylated tau (p-tau) predicted cognitive performance in middle-aged PWH. Methods: In a prospectively followed, cognitively-characterized autopsy sample of 135 PWH, we used immunohistochemistry to assess Aβ plaques and neuronal p-tau in medial temporal and lateral frontal lobes. These pathologies were tested for associations with cognitive performance in seven domains: motor, speed of information processing, working memory, memory encoding, memory retrieval, verbal fluency, and abstraction/executive function. Univariate and multivariate analyses accounting for HIV-associated variables, reading level, and comorbidities were conducted. Longitudinal trajectories of memory functions were evaluated in 60 individuals with a median follow-up of 6.0 years. Results: In this population with mean age 51.4 ± 0.9 years, 58% displayed neuronal p-tau and 29% Aβ plaques. Neuronal p-tau, but not Aβ, predicted worse memory encoding and retrieval, but not other cognitive functions. With an ordinal hierarchy of neuronal p-tau locations (entorhinal, hippocampal, neocortical), decreased memory performance correlated with neocortical distribution. Memory function trajectories could not be distinguished between individuals with and without neuronal p-tau, and over 80% of the sample showed no change over time. Conclusion: In this middle-aged sample, neuronal p-tau accumulation contributes to memory deficits, but is not associated with accelerated decline in function over time. In the absence of AD-like deterioration, other etiologies for neuronal p-tau in cognitively impaired PWH must be considered.
MeSH term(s)	Middle Aged ; Humans ; tau Proteins ; HIV Infections/complications ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Memory Disorders ; Cognitive Dysfunction ; Memory, Short-Term ; Positron-Emission Tomography
Chemical Substances	tau Proteins ; Amyloid beta-Peptides
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000003556
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Article ; Online: The Frequency of Cerebral Amyloid Angiopathy in Primary Age-Related Tauopathy.

Walker, Jamie M / Richardson, Timothy E / Farrell, Kurt / White Iii, Charles L / Crary, John F

Journal of neuropathology and experimental neurology

2022 Volume 81, Issue 3, Page(s) 246–248

MeSH term(s)	Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Humans ; Magnetic Resonance Imaging ; Tauopathies
Language	English
Publishing date	2022-01-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlab131
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Article: Chronic Traumatic Encephalopathy and Neuropathological Comorbidities

Stein, Thor D. / Crary, John F.

Seminars in Neurology

(Chronic Traumatic Encephalopathy)

2020 Volume 40, Issue 04, Page(s) 384–393

Series title	Chronic Traumatic Encephalopathy
Abstract	With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of many neurodegenerative diseases, including chronic traumatic encephalopathy (CTE), Alzheimer's disease, Lewy body disease, and amyotrophic lateral sclerosis, it is becoming critical to understand the relationship and interactions between these pathologies. In fact, comorbid pathology is common in CTE and likely influenced by both age and the severity and type of exposure to RHI as well as underlying genetic predisposition. Here, we review the major comorbid pathologies seen with CTE and in former contact sports athletes and discuss what is known about the associations between RHI, age, and the development of neuropathologies. In addition, we examine the distinction between CTE and age-related pathology including primary age-related tauopathy and age-related tau astrogliopathy.
Keywords	chronic traumatic encephalopathy ; traumatic brain injury ; neurodegenerative disease ; Alzheimer's disease ; comorbidity
Language	English
Publishing date	2020-06-30
Publisher	Thieme Medical Publishers
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713628
Database	Thieme publisher's database

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