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Article ; Online: The Added Value of Tau-PET in the Assessment of Progressive Supranuclear Palsy.

López-Mora, Diego Alfonso / Fernández León, Alejandro / Lleó, Alberto / Blesa, Rafael / Camacho, Valle

2020 Volume 45, Issue 5, Page(s) e239–e240

Abstract: Progressive supranuclear palsy (PSP) is rare neurodegenerative disorder characterized by deposition of fibrillar aggregates of 4R tau-protein in neurons and glial cells. This disorder is underdiagnosed due to the overlap of the clinical syndrome with ... ...

Abstract	Progressive supranuclear palsy (PSP) is rare neurodegenerative disorder characterized by deposition of fibrillar aggregates of 4R tau-protein in neurons and glial cells. This disorder is underdiagnosed due to the overlap of the clinical syndrome with other related conditions. The clinical manifestations include cognitive impairment associated with behavioral changes, akinetic rigid syndrome, and prominent oculomotor dysfunction. We present the F-FDG and F-THK5351 PET images of a 71-year-old man diagnosed of probable PSP. This image highlights the hopeful results of the new tau-PET ligands radiotracers, because it allows to assess the distribution of tau-protein over time, closely associated with neurodegeneration in PSP.
MeSH term(s)	Aged ; Aminopyridines ; Fluorodeoxyglucose F18 ; Humans ; Male ; Positron-Emission Tomography ; Quinolines ; Supranuclear Palsy, Progressive/diagnostic imaging ; Supranuclear Palsy, Progressive/metabolism ; tau Proteins/metabolism
Chemical Substances	Aminopyridines ; Quinolines ; THK5351 ; tau Proteins ; Fluorodeoxyglucose F18 (0Z5B2CJX4D)
Language	English
Publishing date	2020-03-09
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	197628-x
ISSN	1536-0229 ; 0363-9762
ISSN (online)	1536-0229
ISSN	0363-9762
DOI	10.1097/RLU.0000000000002977
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Article: Noncognitive symptoms and long-term treatment expectations for Alzheimer disease.

Blesa, Rafael

Alzheimer disease and associated disorders

2004 Volume 18 Suppl 1, Page(s) S9–16

Abstract: Alzheimer disease (AD) is characterized by both cognitive and noncognitive symptoms that can lead to functional impairment, increased caregiver burden, and institutionalization. Pharmacologic therapies traditionally used to treat cognitive symptoms of AD ...

Abstract	Alzheimer disease (AD) is characterized by both cognitive and noncognitive symptoms that can lead to functional impairment, increased caregiver burden, and institutionalization. Pharmacologic therapies traditionally used to treat cognitive symptoms of AD may prevent and/or control many noncognitive symptoms as well. The acetylcholinesterase inhibitors (AChEIs) galantamine, rivastigmine, and donepezil have been shown to maintain or improve function for at least 1 year. They also have been shown to improve or delay the onset of neuropsychiatric and behavioral symptoms. These noncognitive benefits can impact greatly the lives of patients with AD as well as the persons who care for them.
MeSH term(s)	Activities of Daily Living/classification ; Aged ; Alzheimer Disease/diagnosis ; Alzheimer Disease/drug therapy ; Carbamates/adverse effects ; Carbamates/therapeutic use ; Cholinesterase Inhibitors/adverse effects ; Cholinesterase Inhibitors/therapeutic use ; Donepezil ; Galantamine/adverse effects ; Galantamine/therapeutic use ; Geriatric Assessment/statistics & numerical data ; Humans ; Indans/adverse effects ; Indans/therapeutic use ; Long-Term Care ; Mental Disorders/diagnosis ; Mental Disorders/drug therapy ; Neuropsychological Tests/statistics & numerical data ; Nootropic Agents/adverse effects ; Nootropic Agents/therapeutic use ; Phenylcarbamates ; Piperidines/adverse effects ; Piperidines/therapeutic use ; Rivastigmine ; Thienamycins
Chemical Substances	Carbamates ; Cholinesterase Inhibitors ; Indans ; Nootropic Agents ; Phenylcarbamates ; Piperidines ; Thienamycins ; Galantamine (0D3Q044KCA) ; Donepezil (8SSC91326P) ; Rivastigmine (PKI06M3IW0) ; biapenem (YR5U3L9ZH1)
Language	English
Publishing date	2004-07-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Review
ZDB-ID	1002700-2
ISSN	1546-4156 ; 0893-0341
ISSN (online)	1546-4156
ISSN	0893-0341
DOI	10.1097/01.wad.0000127494.03150.f8
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Zs.A 2569: Show issues

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Article ; Online: Strategies for Continued Successful Treatment in Patients with Alzheimer's Disease: An Overview of Switching Between Pharmacological Agents.

Blesa, Rafael / Toriyama, Kazuhiro / Ueda, Kengo / Knox, Sean / Grossberg, George

Current Alzheimer research

2018 Volume 15, Issue 10, Page(s) 964–974

Abstract: Introduction: Alzheimer's disease (AD) is the most common cause of dementia, characterized by a progressive decline in cognition and function. Current treatment options for AD include the cholinesterase inhibitors (ChEIs) donepezil, galantamine, and ... ...

Abstract	Introduction: Alzheimer's disease (AD) is the most common cause of dementia, characterized by a progressive decline in cognition and function. Current treatment options for AD include the cholinesterase inhibitors (ChEIs) donepezil, galantamine, and rivastigmine, as well as the N-methyl-Daspartate receptor antagonist memantine. Treatment guidelines recommend the use of ChEIs as the standard of care first-line therapy. Several randomized clinical studies have demonstrated the benefits of ChEIs on cognition, global function, behavior and activities of daily living. However, patients may fail to achieve sustained clinical benefits from ChEIs due to lack/loss of efficacy and/or safety, tolerability issues, and poor adherence to the treatment. The purpose of this review is to explore the strategies for continued successful treatment in patients with AD. Methods: Literature search was performed for articles published in PubMed and MEDLINE, using prespecified search terms. Articles were critically evaluated for inclusion based on their titles, abstracts, and full text of the publication. Results and conclusion: The findings of this review indicate that dose up-titration and switching between ChEIs may help to improve response to ChEI treatment and also address issues such as lack/loss of efficacy or safety/tolerability in patients with AD. However, well-designed studies are needed to provide robust evidence.
MeSH term(s)	Activities of Daily Living/psychology ; Alzheimer Disease/complications ; Alzheimer Disease/drug therapy ; Alzheimer Disease/psychology ; Antipsychotic Agents/therapeutic use ; Cognition Disorders/drug therapy ; Cognition Disorders/etiology ; Databases, Bibliographic/statistics & numerical data ; Drug Substitution ; Humans
Chemical Substances	Antipsychotic Agents
Language	English
Publishing date	2018-06-09
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2205170-3
ISSN	1875-5828 ; 1567-2050
ISSN (online)	1875-5828
ISSN	1567-2050
DOI	10.2174/1567205015666180613112040
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Article ; Online: Cortical microinfarcts in adults with Down syndrome assessed with 3T-MRI.

Aranha, Mateus Rozalem / Montal, Victor / van den Brink, Hilde / Pegueroles, Jordi / Carmona-Iragui, Maria / Videla, Laura / Maure Blesa, Lucia / Benejam, Bessy / Arranz, Javier / Valldeneu, Sílvia / Barroeta, Isabel / Fernández, Susana / Ribas, Laia / Alcolea, Daniel / González-Ortiz, Sofía / Bargalló, Núria / Biessels, Geert Jan / Blesa, Rafael / Lleó, Alberto /

Coutinho, Artur Martins / Leite, Cláudia Costa / Bejanin, Alexandre / Fortea, Juan

Alzheimer's & dementia : the journal of the Alzheimer's Association

2024

Abstract: Background: Cortical microinfarcts (CMI) were attributed to cerebrovascular disease and cerebral amyloid angiopathy (CAA). CAA is frequent in Down syndrome (DS) while hypertension is rare, yet no studies have assessed CMI in DS.: Methods: We included ...

Abstract	Background: Cortical microinfarcts (CMI) were attributed to cerebrovascular disease and cerebral amyloid angiopathy (CAA). CAA is frequent in Down syndrome (DS) while hypertension is rare, yet no studies have assessed CMI in DS. Methods: We included 195 adults with DS, 63 with symptomatic sporadic Alzheimer's disease (AD), and 106 controls with 3T magnetic resonance imaging. We assessed CMI prevalence in each group and CMI association with age, AD clinical continuum, vascular risk factors, vascular neuroimaging findings, amyloid/tau/neurodegeneration biomarkers, and cognition in DS. Results: CMI prevalence was 11.8% in DS, 4.7% in controls, and 17.5% in sporadic AD. In DS, CMI increased in prevalence with age and the AD clinical continuum, was clustered in the parietal lobes, and was associated with lacunes and cortico-subcortical infarcts, but not hemorrhagic lesions. Discussion: In DS, CMI are posteriorly distributed and related to ischemic but not hemorrhagic findings suggesting they might be associated with a specific ischemic CAA phenotype. Highlights: This is the first study to assess cortical microinfarcts (assessed with 3T magnetic resonance imaging) in adults with Down syndrome (DS). We studied the prevalence of cortical microinfarcts in DS and its relationship with age, the Alzheimer's disease (AD) clinical continuum, vascular risk factors, vascular neuroimaging findings, amyloid/tau/neurodegeneration biomarkers, and cognition. The prevalence of cortical microinfarcts was 11.8% in DS and increased with age and along the AD clinical continuum. Cortical microinfarcts were clustered in the parietal lobes, and were associated with lacunes and cortico-subcortical infarcts, but not hemorrhagic lesions. In DS, cortical microinfarcts are posteriorly distributed and related to ischemic but not hemorrhagic findings suggesting they might be associated with a specific ischemic phenotype of cerebral amyloid angiopathy.
Language	English
Publishing date	2024-04-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13797
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Article: Cerebrospinal fluid biomarkers for Alzheimer's disease in Down syndrome.

Dekker, Alain D / Fortea, Juan / Blesa, Rafael / De Deyn, Peter P

Alzheimer's & dementia (Amsterdam, Netherlands)

2017 Volume 8, Page(s) 1–10

Abstract: Down syndrome (DS), present in nearly six million people, is associated with an extremely high risk to develop Alzheimer's disease (AD). Amyloid-β and tau pathology are omnipresent from age 40 years onward, but clinical symptoms do not appear in all DS ... ...

Abstract	Down syndrome (DS), present in nearly six million people, is associated with an extremely high risk to develop Alzheimer's disease (AD). Amyloid-β and tau pathology are omnipresent from age 40 years onward, but clinical symptoms do not appear in all DS individuals. Dementia diagnostics is complex in this population, illustrating the great need for predictive biomarkers. Although blood biomarkers have not yet proven useful, cerebrospinal fluid (CSF) biomarkers (low amyloid-β42, high t-tau, and high p-tau) effectively contribute to AD diagnoses in the general population and are increasingly used in clinical practice. Surprisingly, CSF biomarkers have been barely evaluated in DS. Breaking the taboo on CSF analyses would finally allow for the elucidation of its utility in (differential) diagnoses and staging of disease severity. A sensitive and specific biomarker profile for AD in DS would be of paramount importance to daily care, adaptive caregiving, and specific therapeutic interventions.
Language	English
Publishing date	2017-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832898-X
ISSN	2352-8729
ISSN	2352-8729
DOI	10.1016/j.dadm.2017.02.006
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Article: Pathophysiological Underpinnings of Extra-Motor Neurodegeneration in Amyotrophic Lateral Sclerosis: New Insights From Biomarker Studies.

Reyes-Leiva, David / Dols-Icardo, Oriol / Sirisi, Sonia / Cortés-Vicente, Elena / Turon-Sans, Janina / de Luna, Noemi / Blesa, Rafael / Belbin, Olivia / Montal, Victor / Alcolea, Daniel / Fortea, Juan / Lleó, Alberto / Rojas-García, Ricard / Illán-Gala, Ignacio

Frontiers in neurology

2022 Volume 12, Page(s) 750543

Abstract: Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) lie at opposing ends of a clinical, genetic, and neuropathological continuum. In the last decade, it has become clear that cognitive and behavioral changes in patients with ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) lie at opposing ends of a clinical, genetic, and neuropathological continuum. In the last decade, it has become clear that cognitive and behavioral changes in patients with ALS are more frequent than previously recognized. Significantly, these non-motor features can impact the diagnosis, prognosis, and management of ALS. Partially overlapping neuropathological staging systems have been proposed to describe the distribution of TAR DNA-binding protein 43 (TDP-43) aggregates outside the corticospinal tract. However, the relationship between TDP-43 inclusions and neurodegeneration is not absolute and other pathophysiological processes, such as neuroinflammation (with a prominent role of microglia), cortical hyperexcitability, and synaptic dysfunction also play a central role in ALS pathophysiology. In the last decade, imaging and biofluid biomarker studies have revealed important insights into the pathophysiological underpinnings of extra-motor neurodegeneration in the ALS-FTLD continuum. In this review, we first summarize the clinical and pathophysiological correlates of extra-motor neurodegeneration in ALS. Next, we discuss the diagnostic and prognostic value of biomarkers in ALS and their potential to characterize extra-motor neurodegeneration. Finally, we debate about how biomarkers could improve the diagnosis and classification of ALS. Emerging imaging biomarkers of extra-motor neurodegeneration that enable the monitoring of disease progression are particularly promising. In addition, a growing arsenal of biofluid biomarkers linked to neurodegeneration and neuroinflammation are improving the diagnostic accuracy and identification of patients with a faster progression rate. The development and validation of biomarkers that detect the pathological aggregates of TDP-43
Language	English
Publishing date	2022-01-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2021.750543
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Article ; Online: Alzheimer's disease: an evolutionary approach.

Bufill, Enric / Blesa, Rafael / Augustí, Jordi

Journal of anthropological sciences = Rivista di antropologia : JASS

2013 Volume 91, Page(s) 135–157

Abstract: Alzheimer's disease (AD) is a complex disease associated with advanced age whose causes are still not fully known. Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. AD ... ...

Abstract	Alzheimer's disease (AD) is a complex disease associated with advanced age whose causes are still not fully known. Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. AD is very common in humans and extremely uncommon in other mammals, which suggests that the genetic changes underlying the alterations in cerebral structure or function that have taken place over the course of the evolution of the genus Homo have left specific neurons in the human brain particularly vulnerable to factors which trigger the disease. Most of the genes whose mutation leads to AD are involved in synaptic plasticity. Evidence has also been found relating AD to neuronal oxidative stress. Neurons in certain association areas of the human brain retain juvenile characteristics into adulthood, such as the increased expression of genes related to synaptic activity and plasticity, incomplete myelination and elevated aerobic metabolism, which can cause an increase in oxidative stress in these neurons. Oxidative stress can cause myelin breakdown and epigenetic changes in the promoter region of genes related to synaptic plasticity, reducing their expression. These changes may in some cases induce hyperphosphorylation of tau and β-amyloid deposits, which are characteristic of AD. The adaptation of humans to the cognitive niche probably required an increase in synaptic plasticity and activity and neuronal metabolism in neurons in areas related to certain cognitive functions such as autobiographical memory, social interaction and planning. The cost of these changes may have been the brain's increased vulnerability to factors which can trigger AD. This vulnerability may have resulted from the evolutionary legacies that have occurred over the course of the evolution of the human brain, making AD a possible example of antagonistic pleiotropy. The evolutionary approach allows apparently unrelated data from different disciplines to be combined in a manner that may lead to an improved understanding of complex diseases such as Alzheimer's.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/physiopathology ; Cell Adhesion Molecules, Neuronal ; Epigenomics ; Evolution, Molecular ; Extracellular Matrix Proteins ; Genetic Pleiotropy ; Humans ; Nerve Tissue Proteins ; Neuronal Plasticity ; Serine Endopeptidases
Chemical Substances	Cell Adhesion Molecules, Neuronal ; Extracellular Matrix Proteins ; Nerve Tissue Proteins ; Serine Endopeptidases (EC 3.4.21.-) ; reelin protein (EC 3.4.21.-)
Language	English
Publishing date	2013
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2543441-X
ISSN	2037-0644 ; 1827-4765
ISSN (online)	2037-0644
ISSN	1827-4765
DOI	10.4436/jass.91001
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Article ; Online: AMYQ: An index to standardize quantitative amyloid load across PET tracers.

Pegueroles, Jordi / Montal, Victor / Bejanin, Alexandre / Vilaplana, Eduard / Aranha, Mateus / Santos-Santos, Miguel Angel / Alcolea, Daniel / Carrió, Ignasi / Camacho, Valle / Blesa, Rafael / Lleó, Alberto / Fortea, Juan

Alzheimer's & dementia : the journal of the Alzheimer's Association

2021 Volume 17, Issue 9, Page(s) 1499–1508

Abstract: Introduction: Positron emission tomography (PET) amyloid quantification methods require magnetic resonance imaging (MRI) for spatial registration and a priori reference region to scale the images. Furthermore, different tracers have distinct thresholds ... ...

Abstract	Introduction: Positron emission tomography (PET) amyloid quantification methods require magnetic resonance imaging (MRI) for spatial registration and a priori reference region to scale the images. Furthermore, different tracers have distinct thresholds for positivity. We propose the AMYQ index, a new measure of amyloid burden, to overcome these limitations. Methods: We selected 18F-amyloid scans from ADNI and Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL) with the corresponding T1-MRI. A subset also had neuropathological data. PET images were normalized, and the AMYQ was calculated based on an adaptive template. We compared AMYQ with the Centiloid scale on clinical and neuropathological diagnostic performance. Results: AMYQ was related with amyloid neuropathological burden and had excellent diagnostic performance to discriminate controls from patients with Alzheimer's disease (AD) (area under the curve [AUC] = 0.86). AMYQ had a high agreement with the Centiloid scale (intraclass correlation coefficient [ICC] = 0.88) and AUC between 0.94 and 0.99 to discriminate PET positivity when using different Centiloid cutoffs. Discussion: AMYQ is a new MRI-independent index for standardizing and quantifying amyloid load across tracers.
MeSH term(s)	Aged ; Alzheimer Disease/metabolism ; Amyloid/metabolism ; Australia ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Neuropathology ; Positron-Emission Tomography/standards ; United States
Chemical Substances	Amyloid
Language	English
Publishing date	2021-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12317
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Article: Correction: Plasma glial fibrillary acidic protein and neurofilament light chain for the diagnostic and prognostic evaluation of frontotemporal dementia.

Translational neurodegeneration

2023 Volume 12, Issue 1, Page(s) 21

Language	English
Publishing date	2023-05-09
Publishing country	England
Document type	Published Erratum
ZDB-ID	2653701-1
ISSN	2047-9158
ISSN	2047-9158
DOI	10.1186/s40035-023-00351-3
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Article ; Online: Cross-sectional versus longitudinal cognitive assessments for the diagnosis of symptomatic Alzheimer's disease in adults with Down syndrome.

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 9, Page(s) 3916–3925

Abstract: Background: Down syndrome (DS) is a genetic form of Alzheimer's disease (AD). However, clinical diagnosis is difficult, and experts emphasize the need for detecting intra-individual cognitive decline.: Objective: To compare the performance of ... ...

Abstract	Background: Down syndrome (DS) is a genetic form of Alzheimer's disease (AD). However, clinical diagnosis is difficult, and experts emphasize the need for detecting intra-individual cognitive decline. Objective: To compare the performance of baseline and longitudinal neuropsychological assessments for the diagnosis of symptomatic AD in DS. Methods: Longitudinal cohort study of adults with DS. Individuals were classified as asymptomatic, prodromal AD, or AD dementia. We performed receiver operating characteristic curve analyses to compare baseline and longitudinal changes of CAMCOG-DS and mCRT. Results: We included 562 adults with DS. Baseline assessments showed good to excellent diagnostic performance for AD dementia (AUCs between 0.82 and 0.99) and prodromal AD, higher than the 1-year intra-individual cognitive decline (area under the ROC curve between 0.59 and 0.79 for AD dementia, lower for prodromal AD). Longer follow-ups increased the diagnostic performance of the intra-individual cognitive decline. Discussion: Baseline cognitive assessment outperforms the 1-year intra-individual cognitive decline in adults with DS.
MeSH term(s)	Adult ; Humans ; Alzheimer Disease/diagnosis ; Alzheimer Disease/psychology ; Down Syndrome/complications ; Down Syndrome/diagnosis ; Down Syndrome/genetics ; Longitudinal Studies ; Cross-Sectional Studies ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/psychology ; Neuropsychological Tests ; Cognition
Language	English
Publishing date	2023-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13073
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