Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05
  • 2024-06
  • 2024-07
  • br Discussion The present understanding is that patients suf

    2024-07-09


    Discussion The present understanding is that patients suffering from AD are at a higher risk for epilepsy than individuals without AD [[1], [2]]. The clinical diagnostic accuracy of AD has improved significantly during the last decades. However, most of the epidemiological studies on these two often interlinked disorders have not included a full post mortem examination of the brain. Therefore, some of the studies lack the verification of the exact cause of clinical dementia. In this clinicopathological study including a systematic neuropathological evaluation we evaluated the characteristics of 64 subjects with neuropathologically verified AD and assessed the subjects especially for concomitant epilepsy. Our main finding is that 17% with neuropathologically verified AD and possible concomitant neurodegenerative pathology had a history of epileptic seizures. Thus, the prevalence of epilepsy is comparable to previous studies [[1], [2]] and was interestingly identical to a previous clinicopathological study including 446 patients with neuropathologically verified AD [10]. It is necessary to point out that the clinical and clinicopathological studies are not directly comparable due to the lack of post mortem examination in many studies revealing the neuropathology causing dementia. Concomitant pathology, i.e. AD/LBD, AD/VaD been shown to be a common finding in elderly subjects with AD [11] and in line with this, concomitant neuropathological were common both in patients with and without epilepsy. In this clinicopathological study we found that the duration of AD was significantly longer in subjects with AD and epilepsy and they were hospitalized at a younger age. In addition, the age at the time of AD diagnosis was significantly lower in the AD and epilepsy group. This may suggest that the AD progresses more rapidly in the subjects with epilepsy. Previously it has been shown that patients with autosomal dominant early-onset AD present with more frequent seizures than patients with sporadic AD [12]. Howerver, in our study the frequency of the ApoE4 allele, which is a well characterized risk factor for earlier onset AD, and the load of β-amyloid as well as well as the other ccr2 inhibitor did not differ between statistically between the groups. Frequent seizures may possibly lead to faster detoriation of the already fragile neuronal networks of the AD subjects. This may lead to a vicious circle accelerating the underlying neurodegenerative process. Thus, the patients require adequate antiepileptic treatment. In this study, we reported that 17% of elderly subjects with neuropathologically verified AD had a history of epilepsy. We have shown that the patients with both AD and epilepsy differ significantly from the subjects with neuropathology restricted to AD and possible concomitant disease processes. More studies on larger post mortem material are warranted in order to more precisely define the characteristics of this group of AD patients as this may eventually affect the current treatment strategies and lead to a slower cognitive decline.
    Declarations of interest
    Acknowledgments The authors thank the medical laboratory technologists Mrs. Tarja Kauppinen, Mrs. Merja Fali, Mr. Heikki Luukkonen, and Mr. Hannu Tiainen for their skillful technical assistance. Declarations of interest: none. The study was supported by Academy of Finland (A.P.). We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.
    Introduction Parkinson’s and Alzheimer's brain diseases are characterised by uncontrolled muscle activity and deterioration of the general brain functions respectively. Both conditions involve the formation of either changed amounts of normal brain compounds or the appearance of abnormal compounds. For example Parkinson’s disease is considered to originate with a decrease in dopamine formation found in the brain fluids. Effects similar to those of Parkinson’s disease are also induced by a charged molecule 1-methyl-4-phenylpyridinium. Alzheimer’s disease is presently advanced as the formation of a neurotoxic protein in brain fluids as proposed by the amyloid cascade hypothesis [1], [2]. The latter disease is additionally linked to changes in the concentration of various brain compounds such as an increase in the concentration of neurotoxic quinolinic acid [3], [4], [5]. It has also been demonstrated that change in the metabolic content of charged trimethylglycine betaine attenuates induced memory alterations in animals similar to those observed in Alzheimer's disease [1], [2], [3], [4], [5], [6], [7], [8]. The latter observation indicates a link between charged organic compounds and the information supplied by the sensory organs cells to brain cells and the reverse. The linear compounds creatine, creatinine, acetylcholine and urea are present in both brain and muscle cells and are products of charged phosphagen betaine. This presents the possibility that these two cell types are linked by cell generated common physical and chemical effects. Both of these relationships have been shown to give rise to mechanisms of brain operation which are in agreement with observations [9], [10]. Alterations in concentrations of iron compounds in the brain fluids linked to these diseases have been extensively studied. [11], [12]. In this work it is proposed that these diseases develop as a result of changes in the activities and control mechanisms of biochemicals responsible for initiating and continuing the production of cell products.