Please leave your thoughts and comments twila nash my husband was diagnosed with what this certain Dr. He is now 68 and I really only have noticed a striking difference in the last years. He forgets practically everything.
Received Feb 2; Accepted Mar 5. This article has been cited by other articles in PMC. There is still controversy over the role of amyloid in the pathological process. A question arises whether amyloid is responsible for the neurodegeneration or if it accumulates because of the neurodegeneration.
Nowadays, a handful of researchers share a newly emerged view that the ischemic episodes of brain best describe the pathogenic cascade, which eventually leads to neuronal loss, especially in hippocampus, with amyloid accumulation, tau protein pathology and irreversible dementia of Alzheimer type.
The most persuasive evidences come from investigations of ischemically damaged brains of patients and from experimental ischemic brain studies that mimic Alzheimer-type dementia. Also, the progressive damage in the hippocampus [ 4 — 7 ] and the white matter [ 589 ] were found, following brain ischemia.
Transient brain ischemia resulted in an insidious delayed death of specific vulnerable pyramidal neurons within the CA1 subfield of the hippocampus, associated with inflammation [ 4 — 610 ]. White matter changes are characteristic for elderly persons and individuals with cognitive impairment.
Both illnesses affect multiple neuronal systems and involve abnormal aggregation and deposition of potentially dangerous proteins in selected neuronal types.
In both disorders the vulnerability of specific neuron groups is reflected in a characteristic topographical distribution pattern of the lesions throughout the brain cortex and hippocampus, which remains remarkably consistent across cases.
It is difficult to address this problem in human studies and impossible in cultured neurons. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia [ 3426 ]. In the face of new interesting findings, in this review we will try to put all this information together from a genetic point of view.
The postischemic data suggest that ischemia influences amyloid precursor protein mRNA expression, which may contribute directly or indirectly to the deterioration of cognitive deficits in the postischemic period [ 4243 ]. Following ischemia, only the Kunitz protease inhibitor bearing isoform was increased.
In persistent focal ischemic brain injury, amyloid precursor protein mRNA species, which contain a Kunitz-type protease inhibitor domain, were induced in the cortex by day 21 of postischemia but the total amount of precursor mRNA did not change.
This study suggests a selective role of amyloid precursor protein species that contain the Kunitz protease inhibitor domain in molecular mechanisms of postischemic brain injury [ 45 ].
However, estrogen treatment decreased the amyloid precursor protein mRNA upregulation in these areas [ 42 ]. These data apparently demonstrate that estrogen may have an important role in reducing the upregulation of amyloid precursor protein mRNA in the postischemic period. Presenilins The products of the genes on chromosomes 14 and 1 were termed presenilin 1 and presenilin 2, respectively.
Postischemic upregulation of presenilin 1 gene in neurons of the CA3 subfield of hippocampus and dentate gyrus was demonstrated [ 47 ]. Interestingly, a presenilin 1 mRNA reached the highest level on day 3 postischemia in affected areas.
These data suggest that the upregulation of presenilin 1 mRNA may be associated with response of neurons injured by ischemia. In another study, the upregulation of presenilin mRNA was noted in the hippocampus, brain cortex and striatum, following ischemia [ 48 ].
Presenilin mRNA demonstrated the maximal rise in the hippocampus and brain cortex. The overexpression was larger on the contralateral side to the focal ischemic injury. This difference may reflect a loss of brain cells expressing presenilin genes on the ipsilateral side.
Apolipoproteins The apolipoprotein E gene is located on chromosome An increase in astrocytic apolipoprotein E mRNA expression, with the highest level on day 7 postischemia was noted, which suggests that ischemic neuronal injury results in the induction of certain genes within reactive astrocytes and this induction may be partly involved in the postischemic amyloidogenesis [ 49 ].
Postischemic apolipoprotein E mRNA upregulation in glia but not in neurons was seen in penumbra with a peak on the 21st day. In ischemic core, the significant apolipoprotein E mRNA upregulation was found in macrophages [ 50 ].The study of sporadic Alzheimer's disease etiology, now more than ever, needs an infusion of new concepts.
Despite ongoing interest in Alzheimer's disease, the basis of this entity is not yet clear.
At present, the best-established and accepted "culprit" in Alzheimer's disease pathology by most scientists is the amyloid, as the main molecular. Familial Alzheimer’s disease is an exceedingly rare form of Alzheimer’s, that was recently brought to light by the film, “Still Alice.” Learn more about the heartbreaking disease that devastates families and how you can determine your own risk.
NEUROLOGY ; Whether all etiologic forms of Alzheimer's disease (AD) share a final common pathway is a major urbanagricultureinitiative.com determined the severity and regional distribution of neuronal loss, amyloid plaques, neuritic plaques (NPs), and neurofibrillary tangles (NFTs), and calculated the ratio of neuronal loss to NPs and NFTs in brains.
The increasing prevalence of Alzheimer's disease (AD) and a lack of effective prevention or disease-modifying therapies are global challenges with . Sporadic Alzheimer's disease (AD) and type 2 diabetes (T2D), two chronic age-related disorders, have attained epidemic proportions.
In , an estimated million people worldwide were living with dementia; AD being the . • Familial Alzheimer’s disease has the same symptoms as sporadic Alzheimer’s disease and can develop at any age. • Familial Alzheimer’s disease accounts for less than 1% of all cases of Alzheimer’s disease.