Clinical Study of Memory Disorders in Aging Patients with Associated Cardiovascular, Neurological, Neurobehavioral and Metabolic Diseases”. A Review

We have observed semantic memory and episodic memory disorders (100%) in patients ranging from 40 to 92 years-old, associated to cardiovascular diseases and blood hypertension (82%), sleep disorders (50%), neurobehavioral disorders (44%), such as depression, anxiety, aggression, and vascular demencia, disorders of language (36%), neurosensory disorders (28%), as diminution of visual and hearing acuity, dizziness (26%), Parkinson disease (34%), Alzheimer disease (21%), gait disturbances (10%), vertigo (10%), cervicalgia and cervicogenic headache (10%) trigeminal neuralgia (2%,), We observed as comorbidities the following non-nervous diseases: metabolic diseases as diabetes (21%) and hypothyroidism (5%), gastrointestinal pathology (21%), such as constipation, loss of sphincter control, and gastritis, arthritis (13%), prostatic hypertrophy (1%) and loss of weight (1%). We consider that according to their high frequency the most risk factors associated to memory disorders are cardiovascular diseases and blood hypertension (82%), sleep disorders (50%), neurobehavioral disorders (44%), such as depression, anxiety, aggression, and vascular demencia, disorders of language (36%), neurosensory disorders (28%), as diminution of visual and hearing acuity, dizziness (26%), and Parkinson disease (34%)

Preinduction of HSP70 promotes hypoxic tolerance and facilitates acclimatization to acute hypobaric hypoxia in mouse brain

It has been shown that induction of HSP70 by administration of geranylgeranylacetone (GGA) leads to protection against ischemia/reperfusion injury. The present study was performed to determine the effect of GGA on the survival of mice and on brain damage under acute hypobaric hypoxia. The data showed that the mice injected with GGA survived significantly longer than control animals (survival time of 9.55 ± 3.12 min, n = 16 vs. controls at 4.28 ± 4.29 min, n = 15, P < 0.005). Accordingly, the cellular necrosis or degeneration of the hippocampus and the cortex induced by sublethal hypoxia for 6 h could be attenuated by preinjection with GGA, especially in the CA2 and CA3 regions of the hippocampus. In addition, the activity of nitric oxide synthase (NOS) of the hippocampus and the cortex was increased after exposure to sublethal hypoxia for 6 h but could be inhibited by the preinjection of GGA. Furthermore, the expression of HSP70 was significantly increased at 1 h after GGA injection. These results suggest that administration of GGA improved survival rate and prevented acute hypoxic damage to the brain and that the underlying mechanism involved induction of HSP70 and inhibition of NOS activity