Summary of diencephalon

  • thalamus gateway to the cortex containa s number of nuclei mediating sensation motot cortical arousal learining memebry
  • hypothalamus autonomic control endocrine center for emotional resonse
  • pineal gland produces melatonin contains calcium salts

visual processing

the half of your eye which is closes to the nose is nasal retina and the lateral side is temporal retina.

the left nasal and right temporal both see left side of the world and then from there both report to right side of occipital lobe

the contralateral side crosses at optic chiasma

primary visual corted

  • basic information conscious perception of visual images visual association areas
  • processes visual inforamtion concerned with form volour and movement complex visual processing
  • ventral temporal lobe- what am i seeing
  • parietal cortex - where am i seeing it
  • frontal cortex - using it to guide movement

Overall objectives

  • Be able to identify and describe the key structiues involved in learning and memory particularly the hippo campus
  • Alzheimers disease
    • brain regions affected pathological hallmarks, amyloid cascade hypothesis, challanges

memory

episodic memory - personal epidosea in time and space relies on hippo campus

hippocampus the location of the hippocampus medially traces the inferior lateral ventricle horns

fimbria are fibres which connect the hippocampus to other stuff fimbria crus body columns

mamillary bodies are of the hypothalamus and columns connect to these

medial temporal lobe houses the parahippocampad gyrus

the hippocampus has the dentate gyrus, CA fields subiculum and pre-subiculum and parasubiculum this gyrus has rhinal sulcus, perirhinal cortex, parahippocampal cortex

Medial temportal lobe memroy system

  • hippocamal fomation (where)
    • hippocampus
      • CA fields
      • Dentate gyrus
    • subiculum
  • parahippocampal region (what)
    • pre- parasubiculum
    • entorhinal cortex
    • perrhinal corted
    • parahippocampal cortex

hippocampal formation and parahippocampal region has interconnections

patient HM has a bilateral mtl resection and developed retrograde and anterograde amnesia

pateind RB sustained cardiac arrest and permanent anterograde amnessia. this was dues to hippocampal ca1 cell loss

Place cells - head direction cells - fires when animal orient its head grid cells-

Alzheimers

Alzheimer disease is a type of dementia it is characterised by increasing memory loss

early warning sympotns

  • memory loss affesting job skills
  • difficult performing familiar tasks
  • problems with languahe
  • disortientation of time and plance
  • poor judgement
  • pronlems with abstract thinking
  • misplacing things
  • changes in mood or behaviour
  • changes in personality
  • loss of initiative

person cannot communicate verbally undersnad words or instriuction recognise seld recognise familt members care for themselces

anantomic changes we see increased brain atrophy and increased ventricles

Neuropathology we see some pathologies called senile plaques and neurofibrillary tangles

these come from amyloid precursor protein this is a membrain protein and can be cleaved through a few wats

  1. non maylogenic processing this is cleavved by a secretase and then gamma secretase
  2. amylofenic prossessing the protein is cleaved by b secretase and this leads to toxic AB protein plaques

tau protein promotes microtubule assembly and stabilisation.

tau can tangle together to form the tangles leading to cell death.

the tangles always occur earlt in the entorhinal and perirhinal cortices then hippo campus then frontal and perietal lobes

amount of tandles parallels the durationa nd severity of the AD

the cerebellum is never affected by tangles and its hard to know ehy

braak stages detail this progression and the clinical changes

time of onset etc

early onset is genetic and is in < 65 yrs

95% of cases are sporadic with age as the primary predictor

amyloid cascade this is a hypothesis on the pathyphysiology leading to AD

challanges in AD lots of challanges to the amyloid cascade hypothesis

and so more research needs to be done

two hit model of AD cerebrovascular damage initially is the source of neuronal injury and neurodegeration but promotes accumulation of AB toxin ( 2nd hit.)

no cure for AD treatments include

early biomarkers can serve to be early detection points

best preventative is lifestyle intervention and promote successful aging