Ca2+-independent binding and cellular expression profiles question a significant role of calmyrin in transduction of Ca2+-signals to Alzheimer's disease-related presenilin 2 in forebrain

BackgroundPatients with Alzheimer's disease show a wide variation in clinical phenotype. Genetic research has been largely concerned with the role of mutations or common variants as risk factors for the disease. Do genetic factors also influence clinical phenotype?AimsTo examine the evidence that genetic factors influence the clinical expression of the disease in addition to influencing risk.MethodA selective review was made of the key literature.ResultsMutations in three genes, coding for amyloid precursor protein, presenilin-1 and presenilin-2, and a common variation (ε4) in another gene, APOE, have been shown to lead to an earlier development of the disease. More recently, genetic association and twin studies have suggested a role for genetic factors in the development of other aspects of clinical phenotype, notably the appearance of non-cognitive symptoms.ConclusionsIn Alzheimer's disease genetic variation influences a number of aspects of clinical phenotype.

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Markers of Alzheimer’s Disease in Primary Visual Cortex in Normal Aging in Mice

BioMed Research International ◽

10.1155/2017/3706018 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 5

Author(s):

Luis Fernando Hernández-Zimbrón ◽

Montserrat Perez-Hernández ◽

Abigail Torres-Romero ◽

Elisa Gorostieta-Salas ◽

Roberto Gonzalez-Salinas ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Visual Cortex ◽

Visual Loss ◽

Healthy Aging ◽

Normal Aging ◽

Aged Mice ◽

Presenilin 2 ◽

Comprehensive Framework

Aging is the principal risk factor for the development of Alzheimer’s disease (AD). The hallmarks of AD are accumulation of the amyloid-β peptide 1–42 (Aβ42) and abnormal hyperphosphorylation of Tau (p-Tau) protein in different areas of the brain and, more recently reported, in the visual cortex. Recently, Aβ42 peptide overproduction has been involved in visual loss. Similar to AD, in normal aging, there is a significant amyloid deposition related to the overactivation of the aforementioned mechanisms. However, the mechanisms associated with visual loss secondary to age-induced visual cortex affectation are not completely understood. Young and aged mice were used as model to analyze the presence of Aβ42, p-Tau, glial-acidic fibrillary protein (GFAP), and presenilin-2, one of the main enzymes involved in Aβ42 production. Our results show a significant increase of Aβ42 deposition in aged mice in the following cells and/or tissues: endothelial cells and blood vessels and neurons of the visual cortex; they also show an increase of the expression of GFAP and presenilin-2 in this region. These results provide a comprehensive framework for the role of Aβ42 in visual loss due to inflammation present with aging and offer some clues for fruitful avenues for the study of healthy aging.

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Advances with Long Non-Coding RNAs in Alzheimer’s Disease as Peripheral Biomarker

Genes ◽

10.3390/genes12081124 ◽

2021 ◽

Vol 12 (8) ◽

pp. 1124

Author(s):

Maria Garofalo ◽

Cecilia Pandini ◽

Daisy Sproviero ◽

Orietta Pansarasa ◽

Cristina Cereda ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Decline ◽

Significant Role ◽

Rna Processing ◽

Diagnostic Biomarkers ◽

Non Coding Rnas ◽

Peripheral Biomarker

One of the most compelling needs in the study of Alzheimer’s disease (AD) is the characterization of cognitive decline peripheral biomarkers. In this context, the theme of altered RNA processing has emerged as a contributing factor to AD. In particular, the significant role of long non-coding RNAs (lncRNAs) associated to AD is opening new perspectives in AD research. This class of RNAs may offer numerous starting points for new investigations about pathogenic mechanisms and, in particular, about peripheral biomarkers. Indeed, altered lncRNA signatures are emerging as potential diagnostic biomarkers. In this review, we have collected and fully explored all the presented data about lncRNAs and AD in the peripheral system to offer an overview about this class of non-coding RNAs and their possible role in AD.

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The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease

Yearbook of Neurology and Neurosurgery ◽

10.1016/s0513-5117(09)79132-x ◽

2009 ◽

Vol 2009 ◽

pp. 149-150

Author(s):

J.P. Blass

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mitochondrial Dynamics

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Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

Pharmacopsychiatry ◽

10.1055/s-0031-1292513 ◽

2011 ◽

Vol 44 (06) ◽

Author(s):

K Lerche ◽

M Willem ◽

K Kleinknecht ◽

C Romberg ◽

U Konietzko ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Hormone Receptor ◽

Receptor Type ◽

Corticotropin Releasing Hormone ◽

Releasing Hormone

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Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

Melatonin Research ◽

10.32794/mr11250059 ◽

2020 ◽

Vol 3 (2) ◽

pp. 216-242 ◽

Cited By ~ 1

Author(s):

Mayuri Shukla ◽

Areechun Sotthibundhu ◽

Piyarat Govitrapong

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Adult Neurogenesis ◽

Adult Brain ◽

Therapeutic Approaches ◽

Therapeutic Implications ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.

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