Abstract
Abstract. Intended as food for thought this revue offers a general orientation on Alzheimer’s disease (AD) with comments on the brain changes and clinical features. But more importantly, it points out recent research findings which may offer new alleys for AD research pertinent to the etiology and pathogenesis of AD and alternatives to the so far rather unfruitful and costly amyloid research trail. This new knowledge thus comes from various fields of research such as epigenetics, pointing to possible environmental etiologic factors. Further exosomes may provide information on the state of the neuronal population for diagnostic purposes and might become useful as carriers of therapeutic substances. The newly disclosed protein complexity of the synapses may harbor a large yet unexplored field for neurochemical research pertinent to the early or likely initial loss of synapses in Alzheimer disease. The finding of a more generalized neuronal gene disturbance in Alzheimer’s disease shifts the focus from age related changes to developmental disturbances and increased neuronal vulnerability. BBB incompetence with a start in the hippocampus has also recently been pointed out and may initiate the degenerative process of Alzheimer’s disease. Finally, recent basic research findings on glial evolution, underscoring the distance between humans and rodents, our prime disease model animal, points to several new unexplored mechanisms, which may be relevant for the understanding of neurodegenerative processes. Also stressed is the need to institute treatment at an early stage of the disease, necessitating research for markers, which will enable a diagnosis way ahead of the widespread damage present at the time of clinical debut.
Original language | English |
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Pages (from-to) | 1-12 |
Journal | Acta Scientiarum Lundensia |
Volume | 2016 |
Issue number | 002 |
Publication status | Published - 2016 |
Subject classification (UKÄ)
- Neurology
Free keywords
- evolution.
- astrocytic syncytium
- synapses
- exosome
- Blood-Brain barrier
- amyloid hypothesis
- Epigenetic factors
- Dementia
- Alzheimer’s disease