Limbic and cerebellar effects in Alzheimer-Perusini’s disease: A physics-inspired approach DOI Creative Commons
Maria Mannone, Norbert Marwan, Peppino Fazio

и другие.

Biomedical Signal Processing and Control, Год журнала: 2024, Номер 103, С. 107355 - 107355

Опубликована: Дек. 30, 2024

Язык: Английский

Curcumin Improves Neurogenesis in Alzheimer’s Disease Mice via the Upregulation of Wnt/β-Catenin and BDNF DOI Open Access
Sheng-Chun Lou,

Danfeng Gong,

Mengting Yang

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(10), С. 5123 - 5123

Опубликована: Май 8, 2024

Adult neurogenesis in the dentate gyrus (DG) is impaired during Alzheimer's disease (AD) progression. Curcumin has been reported to reduce cell apoptosis and stimulate neurogenesis. This study aimed investigate influence of curcumin on adult AD mice its potential mechanism. Two-month-old male C57BL/6J were injected with soluble β-amyloid (Aβ1-42) using lateral ventricle stereolocalization establish models. An immunofluorescence assay, including bromodeoxyuridine (BrdU), doublecortin (DCX), neuron-specific nuclear antigen (NeuN), was used detect hippocampal Western blot an enzyme-linked immunosorbent assay (ELISA) test expression related proteins secretion brain-derived neurotrophic factor (BDNF). A Morris water maze cognitive function mice. Our results showed that administration (100 mg/kg) rescued Aβ1-42 mice, shown as enhanced BrdU+/DCX+ BrdU+/NeuN+ cells DG. In addition, regulated phosphatidylinositol 3 kinase (PI3K)/protein B (Akt) -mediated glycogen synthase kinase-3β (GSK3β) /Wingless/Integrated (Wnt)/β-catenin pathway cyclic adenosine monophosphate response element-binding protein (CREB)/BDNF Inhibiting Wnt/β-catenin depriving BDNF could reverse both upregulated curcumin-treated conclusion, our indicates curcumin, through targeting PI3K/Akt, regulates GSK3β/Wnt/β-catenin CREB/BDNF pathways, improving

Язык: Английский

Процитировано

10

Postmortem imaging reveals patterns of medial temporal lobe vulnerability to tau pathology in Alzheimer’s disease DOI Creative Commons
Sadhana Ravikumar, Amanda E Denning, Sydney Lim

и другие.

Nature Communications, Год журнала: 2024, Номер 15(1)

Опубликована: Июнь 5, 2024

Abstract Our current understanding of the spread and neurodegenerative effects tau neurofibrillary tangles (NFTs) within medial temporal lobe (MTL) during early stages Alzheimer’s Disease (AD) is limited by presence confounding non-AD pathologies two-dimensional (2-D) nature conventional histology studies. Here, we combine ex vivo MRI serial histological imaging from 25 human MTL specimens to present a detailed, 3-D characterization quantitative NFT burden measures in space high-resolution, atlas with cytoarchitecturally-defined subregion labels, that can be used inform future neuroimaging Average maps show clear anterior poster gradient distribution precise, spatial pattern highest levels NFTs found not just transentorhinal region but also cornu ammonis (CA1) subfield. Additionally, identify granular regions where neurodegeneration are likely linked specifically, thus potentially more sensitive as AD biomarkers.

Язык: Английский

Процитировано

5

The subcortical default mode network and Alzheimer’s disease: a systematic review and meta-analysis DOI Creative Commons
Sara Seoane, Martijn P. van den Heuvel, Ángel Acebes

и другие.

Brain Communications, Год журнала: 2024, Номер 6(2)

Опубликована: Янв. 1, 2024

Abstract The default mode network is a central cortical brain suggested to play major role in several disorders and be particularly vulnerable the neuropathological hallmarks of Alzheimer’s disease. Subcortical involvement its alteration disease remains largely unknown. We performed systematic review, meta-analysis empirical validation subcortical healthy adults, combined with analysis areas Our results show that, besides well-known regions, consistently includes namely thalamus, lobule vermis IX right Crus I/II cerebellum amygdala. Network also suggests caudate nucleus. In disease, we observed left-lateralized cluster decrease functional connectivity which covered medial temporal lobe amygdala showed overlap portion covering parts left anterior hippocampus found an increase insula. These confirm consistency contributions adults highlight relevance

Язык: Английский

Процитировано

4

Investigating neuropathological correlates of hyperactive and psychotic symptoms in dementia: a systematic review DOI Creative Commons
G Negro, Michele Rossi, Camillo Imbimbo

и другие.

Frontiers in Dementia, Год журнала: 2025, Номер 4

Опубликована: Янв. 29, 2025

Introduction Behavioral and Psychological Symptoms of Dementia (BPSD) are common neuropsychiatric manifestations that complicate the clinical course dementia impact caregiving. Among these, Hyperactivity–Impulsivity–Irritiability–Disinhibition–Aggression–Agitation (HIDA) Psychosis (P) domains particularly challenging to manage. Despite their prevalence, underlying mechanisms neuropathological correlates, remain poorly understood. This systematic review aims elucidate basis HIDA psychosis domains, exploring whether distinct proteinopathies neural circuit dysfunctions associated with these symptoms. Methods The follows PRISMA guidelines, a search conducted across MEDLINE, CENTRAL, EMBASE databases. Inclusion criteria involved studies neuropathology in individuals dementia. Records were screened using PICO software, data quality was assessed Newcastle-Ottawa Scale (NOS) CARE guidelines. A narrative synthesis due heterogeneity data. Results From 846 records identified, 37 met inclusion criteria. Of 18,823 cases analyzed, most diagnoses Alzheimer's Disease (83.44%), Lewy Bodies (5.37%), Frontotemporal (13.40%). HIDA-P symptoms distributed all diagnoses, agitation (14.00%), delusions (11.60%), disinhibition (7.61%), hallucinations (6.83%) being frequently reported behaviors. primary diagnosis Neuropathologic Change (ADNC), present predominantly intermediate severe forms. analysis revealed co-occurrence multiple proteinopathies, TAUopathy, TDP-43 pathology, Lewy-related pathology (LRP), latter, association ADNC, 15 studies. Discussion linked overlapping involvement different circuits, amygdala broader limbic system. Evidence suggests TAUopathy key brain regions, such as amygdala, central development In contrast, contribution beta-amyloid vascular damage appears marginal genesis psychotic No behavioral symptom is pathognomonic specific proteinopathy; rather, topography severity lesions plays more decisive role than single molecular composition. Systematic registration INPLASY2024100082.

Язык: Английский

Процитировано

0

Role of tau versus TDP‐43 pathology on medial temporal lobe atrophy in aging and Alzheimer's disease DOI Creative Commons
Laura E.M. Wisse, Anika Wuestefeld,

Melissa Murray

и другие.

Alzheimer s & Dementia, Год журнала: 2025, Номер 21(2)

Опубликована: Фев. 1, 2025

Abstract Hippocampal atrophy on magnetic resonance imaging is an important biomarker in Alzheimer's disease (AD). While hippocampal was thought to result from tau tangles AD, different neuropathologies can lead atrophy, especially TAR DNA‐binding protein 43 (TDP‐43) pathology. In this narrative review, we evaluate existing studies the relative contribution of and TDP‐43 pathology medial temporal lobe (MTL) atrophy. We report a clear association both neuropathology with MTL even after correcting for other neuropathologies. Next, discuss potential synergism between timing effects Finally, avenues future research will be discussed. A better understanding interplay their effect help development more specific biomarkers limbic‐predominant age‐related encephalopathy pinpointing optimal testing anti‐tau anti‐TDP‐43 treatments trials. Highlights Both contribute There positive potentially synergism. It unclear if have additive or synergistic The remains unclear. Clarifying improve biomarkers.

Язык: Английский

Процитировано

0

Impact of amygdala functional connectivity on cognitive impairment in Alzheimer’s disease DOI Creative Commons
Ani Kıçık, Elif Kurt, Emre Harı

и другие.

Neurological Sciences, Год журнала: 2025, Номер unknown

Опубликована: Март 8, 2025

Abstract The functional connectivity (FC) of the amygdala in Alzheimer’s disease (AD) and its relationship to cognitive impairment is still not well established. Thus, we examined resting-state FC changes among 21 patients with AD dementia (ADD) 34 individuals amnestic mild (aMCI), compared 33 subjective (SCI), provide insights into association between decline different clinical stages disease. We conducted seed-to-voxel analysis, focused on two functions, episodic memory, face recognition, correlations test scores. demonstrated that left exhibits progressive disruption FC, especially frontal regions aMCI ADD. further identified this disrupted showed significant positive scores from MCI stage onward. Our results indicate may serve as an early marker pattern influence detrimentally affects memory recognition functions. These findings highlight be a critical anatomical region for detecting AD.

Язык: Английский

Процитировано

0

Cross-ancestry and sex-stratified genome-wide association analyses of amygdala and subnucleus volumes DOI
Yuan Ji, Nana Liu,

Yunjun Yang

и другие.

Nature Genetics, Год журнала: 2025, Номер unknown

Опубликована: Март 17, 2025

Язык: Английский

Процитировано

0

Tau-PET pathology in the subregions of the amygdala and its associations with cognitive performance and neuropsychiatric symptoms in autosomal dominant Alzheimer’s disease DOI Creative Commons
Catarina Tristão‐Pereira, Stephanie Langella, Justin S. Sanchez

и другие.

Alzheimer s Research & Therapy, Год журнала: 2025, Номер 17(1)

Опубликована: Март 20, 2025

The amygdala plays a role in behavior and emotional response is vulnerable to Alzheimer's disease (AD) pathology, yet little known about tau accumulation before clinical symptom onset. To investigate whether certain nuclei are particularly degeneration might underlie early neuropsychiatric symptoms AD, we aimed characterize subregional pathology its correlates associations with established biomarkers of AD cognitive-behavioral measures Presenilin-1 E280A mutation carriers autosomal dominant AD. Participants included 25 cognitively unimpaired 37 non-carrier family members from the Colombia-Boston (COLBOS) Biomarker Study. Measures 18F-flortaucipir, 11C-Pittsburgh compound B, Consortium Establish Registry for Disease Word List Learning, Trail Making Test, Geriatric Depression Scale, Anxiety Inventory. We examined group differences levels (whole amygdala, lateral nucleus basal nucleus) analyzed markers measures. Amygdala were higher compared non-carriers. Among carriers, showed greater burden than nucleus, correlated closer estimated age onset increased cortical amyloid. Additionally, both was associated poorer working memory, lower executive function depressive symptoms. However, did not correlate anxiety. Notably, differentiated non-carriers, predictive accuracy when included. These findings suggest that begins while cognitive deficits nuclei's differential vulnerability underscores importance investigating spread within amygdala-associated networks, relative manifestations This study reinforces potential as valuable biomarker preclinical

Язык: Английский

Процитировано

0

Amygdala atrophies in specific subnuclei in preclinical Alzheimer's disease DOI Creative Commons
Yasmine Salman, Thomas Gérard, Lara Huyghe

и другие.

Alzheimer s & Dementia, Год журнала: 2024, Номер unknown

Опубликована: Сен. 10, 2024

Abstract INTRODUCTION Magnetic resonance imaging (MRI) segmentation algorithms make it possible to study detailed medial temporal lobe (MTL) substructures as hippocampal subfields and amygdala subnuclei, offering opportunities develop biomarkers for preclinical Alzheimer's disease (AD). METHODS We identified the MTL significantly associated with tau‐positron emission tomography (PET) signal in 581 non‐demented individuals from Disease Neuroimaging Initiative (ADNI‐3). confirmed our results UCLouvain cohort including 110 by comparing volumes between different visual Braak's stages clinical diagnosis. RESULTS Four subnuclei (cortical, central, medial, accessory basal) were tau amyloid beta‐positive (Aβ+) clinically normal (CN) individuals, while global not. Using data, we observed that both Braak I‐II Aβ+ CN had smaller these no significant difference was structure or other subfields. CONCLUSION Measuring specific early atrophy may serve a marker of tauopathy AD, identifying at risk progression. Highlights Amygdala is not homogeneous Tau pathology specifically, cortical, basal subnuclei. Hippocampal volume AD. Hippocampus CA1‐3 reduced regardless tau.

Язык: Английский

Процитировано

3

Morphometry of medial temporal lobe subregions using high‐resolution T2‐weighted MRI in ADNI3: Why, how, and what's next? DOI Creative Commons
Paul A. Yushkevich,

Ranjit Ittyerah,

Yue Li

и другие.

Alzheimer s & Dementia, Год журнала: 2024, Номер 20(11), С. 8113 - 8128

Опубликована: Сен. 16, 2024

Abstract This paper for the 20th anniversary of Alzheimer's Disease Neuroimaging Initiative (ADNI) provides an overview magnetic resonance imaging (MRI) medial temporal lobe (MTL) subregions in ADNI using a dedicated high‐resolution T2‐weighted sequence. A review work that supported inclusion this modality into Phase 3 is followed by brief description MTL and analysis protocols summary studies have used these data. supplemented new study uses novel surface‐based tools to characterize neurodegeneration across biomarker‐defined AD stages. reveals pattern spreading cortical thinning associated with increasing levels tau pathology presence elevated amyloid beta, apparent epicenters transentorhinal region inferior hippocampal subfields. The concludes outlook 4. Highlights As 3, protocol includes MRI scan optimized subfields subregions. These scans are processed core obtain automatic segmentations derive morphologic measurements. More detailed granular examination response disease progression achieved applying modeling techniques. Surface‐based gray matter loss spatially expanding patterns advancing stages (AD), as defined based on positron emission tomography biomarkers accordance recently proposed criteria. closely align post mortem literature spread pathological AD, supporting role beta driver neurodegeneration.

Язык: Английский

Процитировано

3