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Brain Sciences
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Neuropathology of Alzheimer’s Disease
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Neuropathology of Alzheimer’s Disease

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (20 January 2021) | Viewed by 33082

Special Issue Editors

Dr. Claire Troakes

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Guest Editor
London Neurodegenerative Diseases Brain Bank, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London, SE5 8AF, UK
Interests: neurodegeneration; neuropathology of dementia; brain banking; Alzheimer’s disease; FTLD
Prof. Dr. Safa Al-Sarraj

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Guest Editor
Department of Clinical Neuropathology, King’s College Hospital NHS Foundation Trust, London, SE5 9RS and London Neurodegenerative Diseases Brain Bank, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London, SE5 8AF, UK
Interests: neurodegeneration; neuropathology of dementia; brain banking; head injury; forensic neuropathology
Dr. Andrew King

E-Mail Website
Guest Editor
Department of Clinical Neuropathology, King’s College Hospital NHS Foundation Trust, London, SE5 9RS and London Neurodegenerative Diseases Brain Bank, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London, SE5 8AF, UK
Interests: neurodegeneration; neuropathology of dementia; Alzheimer’s disease; FTLD

Special Issue Information

Dear Colleagues,

It has been over 100 years since Alois Alzheimer’s paper describing the pathological aspects of the neurodegenerative disease that now bears his name; however, there is still a significant amount we do not understand about the disease’s causation, development and potential treatment target areas. Indeed, considering that the main pathological proteins involved in the disease—β-amyloid and hyperphophosphorylated tau—have been known about for some considerable time, there have been disappointing advances in therapeutic intervention. Furthermore, it has also become apparent that there are often more pathological components to many cases of Alzheimer’s disease than purely amyloid plaques and neurofibrillary tangles. The significance of additional amyloid angiopathy, Lewy bodies and TDP-43 in the overall pathological process remains to be established.

Further, although one of the major risk factors in developing the disease is age, there has been much work into trying to un-knot the neuropathological features of the ageing process itself from those of the progressive Alzheimer’s disease.

This Special Issue will bring together papers describing recent advances and techniques in the neuropathological examination of Alzheimer’s disease.

Dr. Claire Troakes
Prof. Dr. Safa Al-Sarraj
Dr. Andrew King
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Alzheimer’s disease
  • Amyloid
  • Tau
  • Neuropathology

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Published Papers (6 papers)

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Research

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16 pages, 4013 KiB  
Article
The Increased Densities, But Different Distributions, of Both C3 and S100A10 Immunopositive Astrocyte-Like Cells in Alzheimer’s Disease Brains Suggest Possible Roles for Both A1 and A2 Astrocytes in the Disease Pathogenesis
by Andrew King, Boglarka Szekely, Eda Calapkulu, Hanan Ali, Francesca Rios, Shalmai Jones and Claire Troakes
Brain Sci. 2020, 10(8), 503; https://doi.org/10.3390/brainsci10080503 - 31 Jul 2020
Cited by 50 | Viewed by 5740
Abstract
There is increasing evidence of astrocyte dysfunction in the pathogenesis of Alzheimer’s disease (AD). Animal studies supported by human post-mortem work have demonstrated two main astrocyte types: the C3 immunopositive neurotoxic A1 astrocytes and the S100A10 immunopositive neuroprotective A2 astrocytes. A1 astrocytes predominate [...] Read more.
There is increasing evidence of astrocyte dysfunction in the pathogenesis of Alzheimer’s disease (AD). Animal studies supported by human post-mortem work have demonstrated two main astrocyte types: the C3 immunopositive neurotoxic A1 astrocytes and the S100A10 immunopositive neuroprotective A2 astrocytes. A1 astrocytes predominate in AD, but the number of cases has been relatively small. We examined post-mortem brains from a larger cohort of AD cases and controls employing C3 and S100 immunohistochemistry to identify the astrocytic subtypes. There were a number of C3 immunopositive astrocyte-like cells (ASLCs) in the control cases, especially in the lower cerebral cortex and white matter. In AD this cell density appeared to be increased in the upper cerebral cortex but was similar to controls in other regions. The S100A10 showed minimal immunopositivity in the control cases in the cortex and white matter, but there was increased ASLC density in upper/lower cortex and white matter in AD compared to controls. In AD and control cases the numbers of C3 immunopositive ASLCs were greater than those for S100A10 ASLCs in all areas studied. It would appear that the relationship between A1 and A2 astrocytes and their possible role in the pathogenesis of AD is complex and requires more research. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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14 pages, 1333 KiB  
Article
Exercise Training Results in Lower Amyloid Plaque Load and Greater Cognitive Function in an Intensity Dependent Manner in the Tg2576 Mouse Model of Alzheimer’s Disease
by Riya Thomas, Scott D. Zimmerman, Kayla M. Yuede, John R. Cirrito, Leon M. Tai, Benjamin F. Timson and Carla M. Yuede
Brain Sci. 2020, 10(2), 88; https://doi.org/10.3390/brainsci10020088 - 8 Feb 2020
Cited by 11 | Viewed by 3673
Abstract
Three months of exercise training (ET) decreases soluble Aβ40 and Aβ42 levels in an intensity dependent manner early in life in Tg2576 mice (Moore et al., 2016). Here, we examined the effects of 12 months of low- and high- intensity exercise [...] Read more.
Three months of exercise training (ET) decreases soluble Aβ40 and Aβ42 levels in an intensity dependent manner early in life in Tg2576 mice (Moore et al., 2016). Here, we examined the effects of 12 months of low- and high- intensity exercise training on cognitive function and amyloid plaque load in the cortex and hippocampus of 15-month-old Tg2576 mice. Low- (LOW) and high- (HI) intensity ET animals ran at speeds of 15 m/min on a level treadmill and 32 m/min at a 10% grade, respectively, for 60 min/day, five days/week, from 3 to 15 months of age. Sedentary mice (SED) were placed on a level, non-moving, treadmill for the same duration. ET mice demonstrated a significantly lower amyloid plaque load in the cortex and hippocampus that was intensity dependent. Improvement in cognitive function, assessed by Morris Water Maze and Novel Object Recognition tests, was greater in the HI group compared to the LOW and SED groups. LOW mice performed better in the initial latency to the platform location during the probe trial of the Morris Water Maze (MWM) test than SED, but not in any other aspect of MWM or the Novel Object Recognition test. The results of this study indicate that exercise training decreases amyloid plaque load in an intensity dependent manner and that high-intensity exercise training improves cognitive function relative to SED mice, but the intensity of the LOW group was below the threshold to demonstrate robust improvement in cognitive function in Tg2576 mice. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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Review

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20 pages, 1055 KiB  
Review
Renal Contributions in the Pathophysiology and Neuropathological Substrates Shared by Chronic Kidney Disease and Alzheimer’s Disease
by Gabriela Dumitrita Stanciu, Daniela Carmen Ababei, Veronica Bild, Walther Bild, Luminita Paduraru, Mihai Marius Gutu and Bogdan-Ionel Tamba
Brain Sci. 2020, 10(8), 563; https://doi.org/10.3390/brainsci10080563 - 17 Aug 2020
Cited by 20 | Viewed by 4184
Abstract
Chronic kidney disease and Alzheimer’s disease are chronic conditions highly prevalent in elderly communities and societies, and a diagnosis of them is devastating and life changing. Demanding therapies and changes, such as non-compliance, cognitive impairment, and non-cognitive anomalies, may lead to supplementary symptoms [...] Read more.
Chronic kidney disease and Alzheimer’s disease are chronic conditions highly prevalent in elderly communities and societies, and a diagnosis of them is devastating and life changing. Demanding therapies and changes, such as non-compliance, cognitive impairment, and non-cognitive anomalies, may lead to supplementary symptoms and subsequent worsening of well-being and quality of life, impacting the socio-economic status of both patient and family. In recent decades, additional hypotheses have attempted to clarify the connection between these two diseases, multifactorial in their nature, but even so, the mechanisms behind this link are still elusive. In this paper, we sought to highlight the current understanding of the mechanisms for cognitive decline in patients with these concurrent pathologies and provide insight into the relationship between markers related to these disease entities and whether the potential biomarkers for renal function may be used for the diagnosis of Alzheimer’s disease. Exploring detailed knowledge of etiologies, heterogeneity of risk factors, and neuropathological processes associated with these conditions opens opportunities for the development of new therapies and biomarkers to delay or slow their progression and validation of whether the setting of chronic kidney disease could be a potential determinant for cognitive damage in Alzheimer’s disease. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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23 pages, 5783 KiB  
Review
The Neuropathological Diagnosis of Alzheimer’s Disease—The Challenges of Pathological Mimics and Concomitant Pathology
by Andrew King, Istvan Bodi and Claire Troakes
Brain Sci. 2020, 10(8), 479; https://doi.org/10.3390/brainsci10080479 - 24 Jul 2020
Cited by 32 | Viewed by 6312
Abstract
The definitive diagnosis of Alzheimer’s disease (AD) rests with post-mortem neuropathology despite the advent of more sensitive scanning and the search for reliable biomarkers. Even though the classic neuropathological features of AD have been known for many years, it was only relatively recently [...] Read more.
The definitive diagnosis of Alzheimer’s disease (AD) rests with post-mortem neuropathology despite the advent of more sensitive scanning and the search for reliable biomarkers. Even though the classic neuropathological features of AD have been known for many years, it was only relatively recently that more sensitive immunohistochemistry for amyloid beta (Aβ) and hyperphosphorylated tau (HP-tau) replaced silver-staining techniques. However, immunohistochemistry against these and other proteins has not only allowed a more scientific evaluation of the pathology of AD but also revealed some mimics of HP-tau pathological patterns of AD, including age-related changes, argyrophilic grain disease and chronic traumatic encephalopathy. It also highlighted a number of cases of AD with significant additional pathology including Lewy bodies, phosphorylated TDP-43 (p-TDP-43) positive neuronal cytoplasmic inclusions and vascular pathology. This concomitant pathology can cause a number of challenges including the evaluation of the significance of each pathological entity in the make-up of the clinical symptoms, and the threshold of each individual pathology to cause dementia. It also raises the possibility of underlying common aetiologies. Furthermore, the concomitant pathologies could provide explanations as to the relative failure of clinical trials of anti-Aβ therapy in AD patients. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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19 pages, 1474 KiB  
Review
Pathophysiological Mechanisms of Cognitive Impairment and Neurodegeneration by Toxoplasma gondii Infection
by Gloria Ortiz-Guerrero, Rodrigo E. Gonzalez-Reyes, Alejandra de-la-Torre, German Medina-Rincón and Mauricio O. Nava-Mesa
Brain Sci. 2020, 10(6), 369; https://doi.org/10.3390/brainsci10060369 - 12 Jun 2020
Cited by 25 | Viewed by 7125
Abstract
Toxoplasma gondii is an obligate intracellular parasite considered one of the most successful pathogens in the world, owing to its ability to produce long-lasting infections and to persist in the central nervous system (CNS) in most warm-blooded animals, including humans. This parasite has [...] Read more.
Toxoplasma gondii is an obligate intracellular parasite considered one of the most successful pathogens in the world, owing to its ability to produce long-lasting infections and to persist in the central nervous system (CNS) in most warm-blooded animals, including humans. This parasite has a preference to invade neurons and affect the functioning of glial cells. This could lead to neurological and behavioral changes associated with cognitive impairment. Although several studies in humans and animal models have reported controversial results about the relationship between toxoplasmosis and the onset of dementia as a causal factor, two recent meta-analyses have shown a relative association with Alzheimer’s disease (AD). AD is characterized by amyloid-β (Aβ) peptide accumulation, neurofibrillary tangles, and neuroinflammation. Different authors have found that toxoplasmosis may affect Aβ production in brain areas linked with memory functioning, and can induce a central immune response and neurotransmitter imbalance, which in turn, affect the nervous system microenvironment. In contrast, other studies have revealed a reduction of Aβ plaques and hyperphosphorylated tau protein formation in animal models, which might cause some protective effects. The aim of this article is to summarize and review the newest data in regard to different pathophysiological mechanisms of cerebral toxoplasmosis and their relationship with the development of AD and cognitive impairment. All these associations should be investigated further through clinical and experimental studies. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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Other

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15 pages, 637 KiB  
Commentary
Enhancing α-secretase Processing for Alzheimer’s Disease—A View on SFRP1
by Bor Luen Tang
Brain Sci. 2020, 10(2), 122; https://doi.org/10.3390/brainsci10020122 - 22 Feb 2020
Cited by 11 | Viewed by 5269
Abstract
Amyloid β (Aβ) peptides generated via sequential β- and γ-secretase processing of the amyloid precursor protein (APP) are major etiopathological agents of Alzheimer’s disease (AD). However, an initial APP cleavage by an α-secretase, such as the a disintegrin and metalloproteinase domain-containing protein ADAM10, [...] Read more.
Amyloid β (Aβ) peptides generated via sequential β- and γ-secretase processing of the amyloid precursor protein (APP) are major etiopathological agents of Alzheimer’s disease (AD). However, an initial APP cleavage by an α-secretase, such as the a disintegrin and metalloproteinase domain-containing protein ADAM10, precludes β-secretase cleavage and leads to APP processing that does not produce Aβ. The latter appears to underlie the disease symptom-attenuating effects of a multitude of experimental therapeutics in AD animal models. Recent work has indicated that an endogenous inhibitor of ADAM10, secreted-frizzled-related protein 1 (SFRP1), is elevated in human AD brains and associated with amyloid plaques in mouse AD models. Importantly, genetic or functional attenuation of SFRP1 lowered Aβ accumulation and improved AD-related histopathological and neurological traits. Given SFRP1′s well-known activity in attenuating Wnt signaling, which is also commonly impaired in AD, SFRP1 appears to be a promising therapeutic target for AD. This idea, however, needs to be addressed with care because of cancer enhancement potentials resulting from a systemic loss of SFRP1 activity, as well as an upregulation of ADAM10 activity. In this focused review, I shall discuss α-secretase-effected APP processing in AD with a focus on SFRP1, and explore the contrasting perspectives arising from the recent findings. Full article
(This article belongs to the Special Issue Neuropathology of Alzheimer’s Disease)
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