Tau Accumulation in Primary Motor Cortex of Variant Alzheimer’s Disease with Spastic Paraparesis

2016 ◽  
Vol 51 (3) ◽  
pp. 671-675 ◽  
Author(s):  
Chul Hyoung Lyoo ◽  
Hanna Cho ◽  
Jae Yong Choi ◽  
Mi Song Hwang ◽  
Sang Kyoon Hong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Spastic Paraparesis

scholarly journals Transcranial Magnetic Stimulation Studies in Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Andrea Guerra ◽  
Federica Assenza ◽  
Federica Bressi ◽  
Federica Scrascia ◽  
Marco Del Duca ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Large Scale ◽  
Primary Motor Cortex ◽  
Brain Aging ◽  
Cortical Excitability ◽  
Neuronal Degeneration

Although motor deficits affect patients with Alzheimer's disease (AD) only at later stages, recent studies demonstrated that primary motor cortex is precociously affected by neuronal degeneration. It is conceivable that neuronal loss is compensated by reorganization of the neural circuitries, thereby maintaining motor performances in daily living. Effectively several transcranial magnetic stimulation (TMS) studies have demonstrated that cortical excitability is enhanced in AD and primary motor cortex presents functional reorganization. Although the best hypothesis for the pathogenesis of AD remains the degeneration of cholinergic neurons in specific regions of the basal forebrain, the application of specific TMS protocols pointed out a role of other neurotransmitters. The present paper provides a perspective of the TMS techniques used to study neurophysiological aspects of AD showing also that, based on different patterns of cortical excitability, TMS may be useful in discriminating between physiological and pathological brain aging at least at the group level. Moreover repetitive TMS might become useful in the rehabilitation of AD patients. Finally integrated approaches utilizing TMS together with others neuro-physiological techniques, such as high-density EEG, and structural and functional imaging as well as biological markers are proposed as promising tool for large-scale, low-cost, and noninvasive evaluation of at-risk populations.

scholarly journals Modulation of Neurolipid Signaling and Specific Lipid Species in the Triple Transgenic Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 22 (22) ◽  
pp. 12256
Author(s):  
Estibaliz González de San Román ◽  
Alberto Llorente-Ovejero ◽  
Jonatan Martínez-Gardeazabal ◽  
Marta Moreno-Rodríguez ◽  
Lydia Giménez-Llort ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acid ◽  
Motor Cortex ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Neurodegenerative Disorder ◽  
Transgenic Mouse Model ◽  
Lipid Species ◽  
Triple Transgenic Mouse

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia in aging populations. Recently, the regulation of neurolipid-mediated signaling and cerebral lipid species was shown in AD patients. The triple transgenic mouse model (3xTg-AD), harboring βAPPSwe, PS1M146V, and tauP301L transgenes, mimics many critical aspects of AD neuropathology and progressively develops neuropathological markers. Thus, in the present study, 3xTg-AD mice have been used to test the involvement of the neurolipid-based signaling by endocannabinoids (eCB), lysophosphatidic acid (LPA), and sphingosine 1-phosphate (S1P) in relation to the lipid deregulation. [35S]GTPγS autoradiography was used in the presence of specific agonists WIN55,212-2, LPA and CYM5442, to measure the activity mediated by CB1, LPA1, and S1P1 Gi/0 coupled receptors, respectively. Consecutive slides were used to analyze the relative intensities of multiple lipid species by MALDI Mass spectrometry imaging (MSI) with microscopic anatomical resolution. The quantitative analysis of the astrocyte population was performed by immunohistochemistry. CB1 receptor activity was decreased in the amygdala and motor cortex of 3xTg-AD mice, but LPA1 activity was increased in the corpus callosum, motor cortex, hippocampal CA1 area, and striatum. Conversely, S1P1 activity was reduced in hippocampal areas. Moreover, the observed modifications on PC, PA, SM, and PI intensities in different brain areas depend on their fatty acid composition, including decrease of polyunsaturated fatty acid (PUFA) phospholipids and increase of species containing saturated fatty acids (SFA). The regulation of some lipid species in specific brain regions together with the modulation of the eCB, LPA, and S1P signaling in 3xTg-AD mice indicate a neuroprotective adaptation to improve neurotransmission, relieve the myelination dysfunction, and to attenuate astrocyte-mediated neuroinflammation. These results could contribute to identify new therapeutic strategies based on the regulation of the lipid signaling in familial AD patients.

A presenilin 1 mutation (Arg278Ser) associated with early onset Alzheimer’s disease and spastic paraparesis

2007 ◽  
Vol 260 (1-2) ◽  
pp. 78-82 ◽  
Author(s):  
Ashok Raman ◽  
Xia Lin ◽  
Mohnish Suri ◽  
Monica Hewitt ◽  
Cris S. Constantinescu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Onset ◽  
Spastic Paraparesis ◽  
Presenilin 1 ◽  
Presenilin 1 Mutation ◽  
Early Onset Alzheimer’S Disease

P8.19 Sensory-motor cortex reorganization in Alzheimer's disease: an MEG study

2011 ◽  
Vol 122 ◽  
pp. S100
Author(s):  
C. Salustri ◽  
F. Tecchio ◽  
F. Zappasodi ◽  
L. Tomasevic ◽  
M. Ercolani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Motor Cortex ◽  
Sensory Motor

scholarly journals Difficult case of a rare form of familial Alzheimer’s disease with PSEN1 P117L mutation

2018 ◽  
Vol 11 (1) ◽  
pp. e226664
Author(s):  
Ana Luísa Rocha ◽  
Andreia Costa ◽  
Maria Carolina Garrett ◽  
Joana Meireles
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
De Novo ◽  
Spastic Paraparesis ◽  
Difficult Case ◽  
Diagnostic Challenge ◽  
Subsequent Investigation ◽  
Neurology Clinic ◽  
Upper Limb Paresis

Less than 10% of Alzheimer’s disease (AD) cases are familial. Presenilin-1 (PSEN1) mutations are the most frequent aetiology and may be associated to atypical neurological manifestations. We report the case of a 27-year-old right-handed man, ensuing with mild cognitive impairment, motor discoordination and axial myoclonus after a parachute accident. At age 32 he was referred to our neurology clinic, presenting cognitive impairment, cerebellar syndrome, axial myoclonus and hypomimia, without other signs of parkinsonism. Because of absence of family history, he was worked up along the line of spinal ataxic disorders. Later, he developed pseudobulbar affect, cognitive deterioration, right upper limb paresis and spastic paraparesis. Subsequent investigation identified a PSEN1 P117L mutation and the diagnosis of autosomal dominant AD was made. This case illustrates the diagnostic challenge imposed by atypical presentation of de novo PSEN1 mutation, leading to unnecessary investigation. Genetic study might be essential for defining the diagnosis.

scholarly journals Gender-Specific Hippocampal Dysrhythmia and Aberrant Hippocampal and Cortical Excitability in the APPswePS1dE9 Model of Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Anna Papazoglou ◽  
Julien Soos ◽  
Andreas Lundt ◽  
Carola Wormuth ◽  
Varun Raj Ginde ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Primary Motor Cortex ◽  
Seizure Activity ◽  
Cortical Excitability ◽  
Memory Loss ◽  
Fast Fourier Transformation ◽  
Model Of Alzheimer’S Disease ◽  
Eeg Recordings ◽  
Gender Specific

Alzheimer’s disease (AD) is a multifactorial disorder leading to progressive memory loss and eventually death. In this study an APPswePS1dE9 AD mouse model has been analyzed using implantable video-EEG radiotelemetry to perform long-term EEG recordings from the primary motor cortex M1 and the hippocampal CA1 region in both genders. Besides motor activity, EEG recordings were analyzed for electroencephalographic seizure activity and frequency characteristics using a Fast Fourier Transformation (FFT) based approach. Automatic seizure detection revealed severe electroencephalographic seizure activity in both M1 and CA1 deflection in APPswePS1dE9 mice with gender-specific characteristics. Frequency analysis of both surface and deep EEG recordings elicited complex age, gender, and activity dependent alterations in the theta and gamma range. Females displayed an antithetic decrease in theta (θ) and increase in gamma (γ) power at 18-19 weeks of age whereas related changes in males occurred earlier at 14 weeks of age. In females, theta (θ) and gamma (γ) power alterations predominated in the inactive state suggesting a reduction in atropine-sensitive type II theta in APPswePS1dE9 animals. Gender-specific central dysrhythmia and network alterations in APPswePS1dE9 point to a functional role in behavioral and cognitive deficits and might serve as early biomarkers for AD in the future.

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