“…It is estimated that AD affects about 11% of individuals aged 65 years or older [ 3 ], whereas iNPH only affects 1.4% of the same population [ 4 ]. Of all patients clinically diagnosed with AD, post-mortem examinations reveal that 10%–20% of these patients have died with conditions other than AD [ 5 ]. Neuropathological examinations reveal that about 56% of patients clinically diagnosed with NPH also suffered AD [ 6 ].…”
ObjectiveIn the present study, cerebrospinal fluid (CSF) profiles were assessed to determine how idiopathic normal pressure hydrocephalus (NPH) and Alzheimer’s disease (AD) differs.MethodsSubjects were drawn from patients who underwent lumbar punctures as part of their diagnostic evaluations in the Banner Sun Health Research Institute Memory Disorders clinic. The clinical sample included 11 iNPH subjects (mean age 81.36±2.58) and 11 AD subjects (mean age 61.46±8.24). Concentrations of amyloid-β (Aβ42), total-tau (t-tau), phospho-tau181 (p-tau) Aβ42, and an Aβ42-Tau Index (ATI) were measured by commercial assay (Athena Diagnostics). and compared to each other. The Mann-Whitney test was used to assess group differences on the raw values for Aβ42, t-tau, p-tau, ATI, age, education, and MMSE.ResultsIn a univariate analysis, p-tau was found to be significantly (P = 0.009) lower in patients diagnosed with iNPH than those with AD. Amyloid-β (Aβ42), total-tau (t-tau) did not differ between groups. In multi-variate analysis, the differences in p-tau between groups did not differ.ConclusionAlthough age could represent a significant confound, p-tau is significantly lower in iNPH compared to AD. P-tau would be expected to increase with age but in this sample is lower suggesting the difference might be explained by the underlying condition.
“…It is estimated that AD affects about 11% of individuals aged 65 years or older [ 3 ], whereas iNPH only affects 1.4% of the same population [ 4 ]. Of all patients clinically diagnosed with AD, post-mortem examinations reveal that 10%–20% of these patients have died with conditions other than AD [ 5 ]. Neuropathological examinations reveal that about 56% of patients clinically diagnosed with NPH also suffered AD [ 6 ].…”
ObjectiveIn the present study, cerebrospinal fluid (CSF) profiles were assessed to determine how idiopathic normal pressure hydrocephalus (NPH) and Alzheimer’s disease (AD) differs.MethodsSubjects were drawn from patients who underwent lumbar punctures as part of their diagnostic evaluations in the Banner Sun Health Research Institute Memory Disorders clinic. The clinical sample included 11 iNPH subjects (mean age 81.36±2.58) and 11 AD subjects (mean age 61.46±8.24). Concentrations of amyloid-β (Aβ42), total-tau (t-tau), phospho-tau181 (p-tau) Aβ42, and an Aβ42-Tau Index (ATI) were measured by commercial assay (Athena Diagnostics). and compared to each other. The Mann-Whitney test was used to assess group differences on the raw values for Aβ42, t-tau, p-tau, ATI, age, education, and MMSE.ResultsIn a univariate analysis, p-tau was found to be significantly (P = 0.009) lower in patients diagnosed with iNPH than those with AD. Amyloid-β (Aβ42), total-tau (t-tau) did not differ between groups. In multi-variate analysis, the differences in p-tau between groups did not differ.ConclusionAlthough age could represent a significant confound, p-tau is significantly lower in iNPH compared to AD. P-tau would be expected to increase with age but in this sample is lower suggesting the difference might be explained by the underlying condition.
“…This methodology has allowed performing comprehensive analysis of changes in transcriptional expression of many genes associated with the pathophysiology of DS [24]. In addition, previous studies have shown the importance of using postmortem brain tissue to analyze the transcriptome of different conditions and different regions of the human brain including those individuals with DS [25]. The gene expression profile of the central nervous system (CNS) is unique.…”
Section: Functional Neurogenomics: the Systemic Integration Of Brain mentioning
Functional neurogenomics is the interface between neurosciences knowledge and Omics sciences data. It characterizes, identifies, and analyzes expression of genes involved in the function of several structures of brain and cognition. Its major goal is to understand the main pathways of brain function, plasticity, and the etiopathogenesis of brain diseases. We have done an integrate analysis of global brain gene expression linked to cognitive disability in Down syndrome. It is a new approach to better understand the control of complex brain networks of gene expression involved in this syndrome. The objective of the chapter is to present computationally simulate data of global expression of 108 genes associated with cognitive disability and neuroplasticity from DNA microarray experiments of postmortem brain from normal controls and patients with Down syndrome. Some genes that were studied are involved in metabolic process and also promote hippocampal plasticity; interventions reawaken the neural plasticity may permit improved cognition. One of the striking findings was that some of the causes of dysregulation appear to result in the brain being trapped in an immature state of synaptic development. Understanding the functional neurogenomics of Down syndrome brain, emerge a new scenario to partially overcome cognitive disability through new prospective genomic therapies.
“…Once identified, biomarkers in dementia will be incorporated into clinical drug trials and will help elucidate the mechanisms of the different dementing conditions as well drug actions. 54 …”
Until recently, the study of cognitive impairment as a manifestation of
cerebrovascular disease (CVD) has been hampered by the lack of common standards
for assessment. The term vascular cognitive impairment (VCI) encompasses all
levels of cognitive decline associated with CVD from mild deficits in one or
more cognitive domains to crude dementia syndrome. VCI incorporates the complex
interactions among classic vascular risk factors (i.e. arterial hypertension,
high cholesterol, and diabetes), CVD subtypes, and Alzheimer’s Disease (AD)
pathology. VCI may be the earliest, commonest, and subtlest manifestation of CVD
and can be regarded as a highly prevalent and preventable
syndrome. However, cognition is not a standardized outcome measure
in clinical trials assessing functional ability after stroke. Furthermore, with
the exception of anti-hypertensive medications, the impact of either preventive
or acute stroke treatments on cognitive outcome is not known. Although clinical,
epidemiological, neuroimaging, and experimental data support the VCI concept,
there is a lack of integrated knowledge on the role played by the most relevant
pathophysiological mechanisms involved in several neurological conditions
including stroke and cognitive impairment such as excitotoxicity, apoptosis,
mitochondrial DNA damage, oxidative stress, disturbed neurotransmitter release,
and inflammation. For this reason, in 2006 the National Institute of
Neurological Disorders and Stroke (NINDS) and the Canadian Stroke Network (CSN)
defined a set of data elements to be collected in future studies aimed at
defining VCI etiology, clinical manifestations, predictive factors, and
treatment. These recommendations represent the first step toward developing
diagnostic criteria for VCI based on sound knowledge rather than on hypotheses.
The second step will be to integrate all studies using the agreed methodologies.
This is likely to accelerate the search for answers.
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