Alzheimer's Factors in Ischemic Brain Injury

Pluta, Ryszard; Jabłoński, Mirosław

doi:10.5772/27205

Cited by 6 publications

(14 citation statements)

References 283 publications

(474 reference statements)

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“…Two days after cardiac arrest, small areas of neuronal disappearance were noted in the selectively vulnerable hippocampus CA1 region [18,20,21]. At 7-14 days, in ischaemic hippocampus neuronal loss was almost complete in CA1 area with single and scattered damaged pyramidal neurons [8,18,20,21].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…At 7-14 days, in ischaemic hippocampus neuronal loss was almost complete in CA1 area with single and scattered damaged pyramidal neurons [8,18,20,21]. But in areas not selectively vulnerable, such as CA2, CA3, and CA4 sectors of the hippocampus, alterations were of a nature characteristic of the acute ischaemic phase [20][21][22]. In different periods following ischaemia, regions of neuronal loss were replaced by proliferating and hypertrophic astrocytes with staining for β-amyloid peptide and microglia [18,19].…”

Section: Discussionmentioning

confidence: 99%

“…Recently it has been identified that degenerative machinery in post-ischaemic neuronal cells continues outside the acute period of the ischaemic episode [18][19][20]. Evidence indicates that post-ischaemic brain injury, regardless of the time of survival after ischaemia, is followed by acute neuronal damage as a "burning phenomenon" in areas of the brain belonging or not to selectively vulnerable regions [18][19][20][21][22].…”

Section: Discussionmentioning

confidence: 99%

“…cortical, neurons also contributing to dysfunction of the neural network. Secondary pathology in the hippocampus in humans and after experimental global cerebral ischaemia due to cardiac arrest occurs with several features similar to Alzheimer's disease [10,20,21,23,24]. The most important similarity is the accumulation of amyloid precursor protein or its fragments, e.g.…”

Section: Introductionmentioning

confidence: 99%

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Occurrence of spontaneous and audiogenic seizures following global brain ischaemia due to cardiac arrest

Ułamek-Kozioł¹,

Kocki²,

Bogucka‐Kocka³

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Occurrence of spontaneous and audiogenic seizures following global brain ischaemia due to cardiac arrest

Ułamek-Kozioł¹,

Kocki²,

Bogucka‐Kocka³

et al. 2015

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Sporadic Alzheimer’s Disease Begins as Episodes of Brain Ischemia and Ischemically Dysregulated Alzheimer’s Disease Genes

et al. 2013

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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 bestestablished and accepted "culprit" in Alzheimer's disease pathology by most scientists is the amyloid, as the main molecular factor responsible for neurodegeneration in this disease. Abnormal upregulation of amyloid production or a disturbed clearance mechanism may lead to pathological accumulation of amyloid in brain according to the "amyloid hypothesis." We will critically review these observations and highlight inconsistencies between the predictions of the "amyloid hypothesis" and the published data. 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. Recent evidence suggests that the pathophysiology and neuropathology of Alzheimer's disease comprises more than amyloid accumulation, tau protein pathology and finally brain atrophy with dementia. Nowadays, a handful

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Brain Ischemia as a Prelude to Alzheimer's Disease

Pluta

Januszewski

Czuczwar

2021

Front. Aging Neurosci.

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Transient ischemic brain injury causes massive neuronal death in the hippocampus of both humans and animals. This was accompanied by progressive atrophy of the hippocampus, brain cortex, and white matter lesions. Furthermore, it has been noted that neurodegenerative processes after an episode of ischemia-reperfusion in the brain can continue well-beyond the acute stage. Rarefaction of white matter was significantly increased in animals at 2 years following ischemia. Some rats that survived 2 years after ischemia developed severe brain atrophy with dementia. The profile of post-ischemic brain neurodegeneration shares a commonality with neurodegeneration in Alzheimer's disease. Furthermore, post-ischemic brain injury is associated with the deposition of folding proteins, such as amyloid and tau protein, in the intracellular and extracellular space. Recent studies on post-ischemic brain neurodegeneration have revealed the dysregulation of Alzheimer's disease-associated genes such as amyloid protein precursor, α-secretase, β-secretase, presenilin 1, presenilin 2, and tau protein. The latest data demonstrate that Alzheimer's disease-related proteins and their genes play a key role in the development of post-ischemic brain neurodegeneration with full-blown dementia in disease types such as Alzheimer's. Ongoing interest in the study of brain ischemia has provided evidence showing that ischemia may be involved in the development of the genotype and phenotype of Alzheimer's disease, suggesting that brain ischemia can be considered as a useful model for understanding the mechanisms responsible for the initiation of Alzheimer's disease.

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Alzheimer's Factors in Ischemic Brain Injury

Cited by 6 publications

References 283 publications

Occurrence of spontaneous and audiogenic seizures following global brain ischaemia due to cardiac arrest

Occurrence of spontaneous and audiogenic seizures following global brain ischaemia due to cardiac arrest

Sporadic Alzheimer’s Disease Begins as Episodes of Brain Ischemia and Ischemically Dysregulated Alzheimer’s Disease Genes

Brain Ischemia as a Prelude to Alzheimer's Disease

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