Introduction: Dementia is basically the DISEASE of old people which is usually caused by a primary degenerative lesion or by a structural DISEASE in the brain. In terms of etiology, dementia is associated with reversible and irreversible causes. Determination of the underlying causes of dementia may facilitate its treatment and prognosis. The purpose of this study is to evaluate clinical and paraclinical symptoms of dementia as well as to determine the most common causes.Materials and Methods: This is a cross sectional descriptive study on 100 patients with dementia who referred to Shahrivar 17th Hospital in Mashhad. First, the patients who were diagnosed as being infected by dementia were evaluated according to DSM-IV criteria. They were also enrolled in history taking and physical examinations as well as paraclinical managements like EEG, CT Scan and MRI.The obtained data were then recorded down in the questionnaires.Results: 36% of the patients were females and 64% were males. Of this population, 43% had Alzheimer DISEASE (AD), 40% had Vascular Dementia (VaD), 9% Parkinson DISEASE (PD) and 8% had other types of dementia while there was no case of Ferontotemporal dementia (FTD). HTN, DM and Hyperlipidemia were found to have a fully significant effect on VaD.100% with the history of TIA and 88% with the history of CVA had VaD which was meaningful, too.55% of the VaD patients were identified with Gait disorder and 65% with Incontinence which is ststistically significant. Based on the results of MRI and CT Scan, 100% of the AD patients, 47.5% of the VaD patients and 88.9% of the PD patients were identified with cortical atrophy. In addition, it was found that hypocampus atrophy was present in 53.5% of the patients with AD and in 15% of the patients with VaD. In 90% of the VaD patients, hypodense foci was observed which is statistically significant, too.Conclusion: As the findings of the study suggest, the results of CT Scan and MRI was notably related to the type of dementia. Thus, it seems that using these two techniques can determine the existence of dementia in the early stages which can help with improving the quality and quantity of life in these patients. According to the frequency rate of VaD in our patients, it seems that the lack of or poor control of the risk factors like HTN, DM and hyperlipidemia can lead to the high frequency rate of vascular dementia.

In the 8th edition (1910) of "Psychiatrie: Ein Lehrbuch fur Studirende und Arzte", Kraepelin stated that a "particular group of cases with extremely serious cell alterations" were discussed by Alzheimer. Those changes were: "Excessively numerous plaques, dying of almost one-third of the cortical cells, and peculiar, deeply stained bundles of neurofibrils in place of them". According to Kraepelin, these changes: "represent the most serious forms of senile dementia". Kraepeline mentioned "ALZHEIMER’S DISEASE" for the first time when he stated that: "The clinical interpretation of this ALZHEIMER’S DISEASE is still unclear". Since that time, there were doubts about the diagnosis of Auguste Deter’s illness (the first case that Alzheimer introduced in 1906), and why did Kraepelin name this condition as ALZHEIMER’S DISEASE. Now after 99 years there seem to be reliable answers to these questions. Description of Auguste Deter’s Dementia by Alzheimer in 1907, and then By Perusini in 1909, indicated the senile plaques and neurofibrillary tangles. Besides, Perusini restudied the brain of this case and found no significant signs of arteriosclerosis. In 1998, scientists at the Max Planck Institue of Neurobiology, Martinsried, Germany, and at the University of Munich, rediscovered brain sections of the first reported case of ALZHEIMER’S DISEASE. Examination of these tissue sections showed a large number of neurofibrillary tangles and amyloid plaques. So, this case represents a typical example of ALZHEIMER’S DISEASE according to today’s standards. It is interesting, too, that in 1997 Dr. Graeber and his colleagues in Max Planck Institute of Psychiatry, Department of Neuromorphology, Martinsried, Germany, had identified well-preserved histological brain sections of ALZHEIMER’S second case, known as Johann F. Examination of the patient’s brain revealed numerous amyloid plaques, but no neurofibrillary tangles in the cerebral cortex, corresponding to a less common form of ALZHEIMER’S DISEASE which may be referred to as "Plaque only". The researchers in Max Planck Institute performed mutational screening of exon 17 of the amyloid precursor protein gene and genotyping for apolipoprotein E alleles. The patient was shown to be homozygous for apolipoprotein E allele epsilon 3 and lacked APP mutations at codons 692, 693, 713 and 717. With regard to the brain sections of Auguste D., genotyping for the apolipoprotein E epsilon 4 allele revealed absence of this ALZHEIMER’S DISEASE "risk factor" but at the same time demonstrated that mutation analysis of the more than 90 years old brain tissue was still feasible. In the hundredth anniversary of Dr. ALZHEIMER’S historical exploration, his findings are newly confirmed.

Alzheimer's DISEASE (AD) is a common cause of dementia in elderly people that is accompanied by progressive cognitive decline and memory loss. The pathologic hallmarks of AD are synaptic and neuronal degeneration together with extracellular senile plaques containing amyloid-beta (Ab) and the intracellular neurofibrillary tangles (NFTs) in the hippocampus and other cortical regions. Amyloid-beta peptide is believed to have a pivotal role in the pathogenesis of AD as a major component of the senile plaques. It acts as a trigger key of AD and is considered as the principal toxic factor in the pathogenesis of the DISEASE.Accumulation of amyloid b protein (Ab), a main component of the senile plaques, in the brain initiates a cascade of events that ultimately lead to neuronal dysfunction and cognitive deficits. Other proposed mechanisms for AD include impairment in cholinergic function, oxidative stress, inflammatory agents and glutamate-mediated excitotoxicity. AD is characterized neuropathologically by impaired cholinergic function, increased oxidative stress, neuroinflammation, neuronal cell death, synapses loss, cortical atrophy, deficiencies in steroid hormones and appearance of glutamate-mediated excitotoxicity.

Alzheimer's DISEASE is an irreversible chronic neurodegenerative DISEASE which is the most common cause of dementia among older adults. According to amyloid hypothesis, cholin neurotransmitters have important roles in CNS memory function, therefore cholinesterase inhibitors can improve the Alzheimer's symptoms. In recent decades, marine creatures have become interested for their huge medicinal effects and potential of pharmaceutical preparations. Marine classifications contain pharmacologically active compounds with capibilities for improvement of cognitive disorders. This article provides a comprehensive overview of cholinesterase inhibitors from marines in 4 categories contain seaweeds, marine sponges, coelenterates and other invertebrates over the 47 years from 1970 to 2017 which resulted into important bioactive extracts and isolated compounds which representing a diverse range of structural classes such as pyrrole derivatives, sesquiterpene acetates, tetrazacyclopentazulene, bromotyrosine derivatives, plastoquinones, farnesylacetones and poly-alkylpyridinium polymers (Poly-APS). For each structural group, the important compounds with cholinesterase inhibition activities were introduced. The result showed marins can be considered as important sources to discover new cholinesterase inhibitiors.